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bibo:doi: 10.1038%2Fs41467-017-00145-y
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Subject Item: _:vb66078360
rdf:type: n5:Section
dc:title: introduction
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Subject Item: _:vb66078361
rdf:type: n2:Context
rdf:value: Cell competition was originally described in Drosophila wing imaginal discs>>1<<; however, it is now clear that it is a universal process, which also occurs in other Drosophila tissues2, 3 including adult tissues4–6, in the mouse embryo7–9, liver10 and heart11 and in mammalian cell culture8, 9, 12, 13.
n2:mentions: n3:1116643

Subject Item: _:vb66078362
rdf:type: n2:Context
rdf:value: Cell competition was originally described in Drosophila wing imaginal discs1; however, it is now clear that it is a universal process, which also occurs in other Drosophila tissues>>2<<, 3 including adult tissues4–6, in the mouse embryo7–9, liver10 and heart11 and in mammalian cell culture8, 9, 12, 13.
n2:mentions: n3:14592975

Subject Item: _:vb66078363
rdf:type: n2:Context
rdf:value: Cell competition was originally described in Drosophila wing imaginal discs1; however, it is now clear that it is a universal process, which also occurs in other Drosophila tissues2, >>3<< including adult tissues4–6, in the mouse embryo7–9, liver10 and heart11 and in mammalian cell culture8, 9, 12, 13.
n2:mentions: n3:23685249

Subject Item: _:vb66078364
rdf:type: n2:Context
rdf:value: Cell competition was originally described in Drosophila wing imaginal discs1; however, it is now clear that it is a universal process, which also occurs in other Drosophila tissues2, 3 including adult tissues>>4<<–6, in the mouse embryo7–9, liver10 and heart11 and in mammalian cell culture8, 9, 12, 13.
n2:mentions: n3:23810538 n3:26853366 n3:26212135

Subject Item: _:vb66078365
rdf:type: n2:Context
rdf:value: Cell competition was originally described in Drosophila wing imaginal discs1; however, it is now clear that it is a universal process, which also occurs in other Drosophila tissues2, 3 including adult tissues4–6, in the mouse embryo>>7<<–9, liver10 and heart11 and in mammalian cell culture8, 9, 12, 13.
n2:mentions: n3:23867226 n3:23842495 n3:15289434

Subject Item: _:vb66078366
rdf:type: n2:Context
rdf:value: competition was originally described in Drosophila wing imaginal discs1; however, it is now clear that it is a universal process, which also occurs in other Drosophila tissues2, 3 including adult tissues4–6, in the mouse embryo7–9, liver>>10<< and heart11 and in mammalian cell culture8, 9, 12, 13. Further studies have also shown the existence of this process in several stem cell compartments14–17, although it is likely that in this case it happens via a different mechanism(s).
n2:mentions: n3:16472603

Subject Item: _:vb66078367
rdf:type: n2:Context
rdf:value: was originally described in Drosophila wing imaginal discs1; however, it is now clear that it is a universal process, which also occurs in other Drosophila tissues2, 3 including adult tissues4–6, in the mouse embryo7–9, liver10 and heart>>11<< and in mammalian cell culture8, 9, 12, 13. Further studies have also shown the existence of this process in several stem cell compartments14–17, although it is likely that in this case it happens via a different mechanism(s).
n2:mentions: n3:25199831

Subject Item: _:vb66078368
rdf:type: n2:Context
rdf:value: wing imaginal discs1; however, it is now clear that it is a universal process, which also occurs in other Drosophila tissues2, 3 including adult tissues4–6, in the mouse embryo7–9, liver10 and heart11 and in mammalian cell culture>>8<<, 9, 12, 13. Further studies have also shown the existence of this process in several stem cell compartments14–17, although it is likely that in this case it happens via a different mechanism(s).
n2:mentions: n3:23867226

Subject Item: _:vb66078369
rdf:type: n2:Context
rdf:value: wing imaginal discs1; however, it is now clear that it is a universal process, which also occurs in other Drosophila tissues2, 3 including adult tissues4–6, in the mouse embryo7–9, liver10 and heart11 and in mammalian cell culture8, >>9<<, 12, 13. Further studies have also shown the existence of this process in several stem cell compartments14–17, although it is likely that in this case it happens via a different mechanism(s).
n2:mentions: n3:23842495

Subject Item: _:vb66078370
rdf:type: n2:Context
rdf:value: wing imaginal discs1; however, it is now clear that it is a universal process, which also occurs in other Drosophila tissues2, 3 including adult tissues4–6, in the mouse embryo7–9, liver10 and heart11 and in mammalian cell culture8, 9, >>12<<, 13. Further studies have also shown the existence of this process in several stem cell compartments14–17, although it is likely that in this case it happens via a different mechanism(s).
n2:mentions: n3:20644714

Subject Item: _:vb66078371
rdf:type: n2:Context
rdf:value: imaginal discs1; however, it is now clear that it is a universal process, which also occurs in other Drosophila tissues2, 3 including adult tissues4–6, in the mouse embryo7–9, liver10 and heart11 and in mammalian cell culture8, 9, 12, >>13<<. Further studies have also shown the existence of this process in several stem cell compartments14–17, although it is likely that in this case it happens via a different mechanism(s).
n2:mentions: n3:27109213

Subject Item: _:vb66078372
rdf:type: n2:Context
rdf:value: Further studies have also shown the existence of this process in several stem cell compartments>>14<<–17, although it is likely that in this case it happens via a different mechanism(s).
n2:mentions: n3:20362536 n3:19211674 n3:20208998 n3:25375180

Subject Item: _:vb66078373
rdf:type: n2:Context
rdf:value: The discovery of cell competition emerged from Drosophila studies of heterozygous mutations in ribosomal genes known as Minute mutations>>18<<. While Minute heterozygous cells and animals are viable, in mosaic tissues Minute heterozygous cells behave as losers and are killed when confronted with wild-type (WT) cells, allowing the healthy WT population to expand efficiently1, 19.
n2:mentions: n3:17927810

Subject Item: _:vb66078374
rdf:type: n2:Context
rdf:value: While Minute heterozygous cells and animals are viable, in mosaic tissues Minute heterozygous cells behave as losers and are killed when confronted with wild-type (WT) cells, allowing the healthy WT population to expand efficiently>>1<<, 19. In addition to Minute, many other mutations have been shown to induce a loser status against WT cells, such as mutations in the oncogene myc 20, in the polarity genes scribble 2, dlg 21 and lgl 22, in the
n2:mentions: n3:1116643

Subject Item: _:vb66078375
rdf:type: n2:Context
rdf:value: While Minute heterozygous cells and animals are viable, in mosaic tissues Minute heterozygous cells behave as losers and are killed when confronted with wild-type (WT) cells, allowing the healthy WT population to expand efficiently1, >>19<<. In addition to Minute, many other mutations have been shown to induce a loser status against WT cells, such as mutations in the oncogene myc 20, in the polarity genes scribble 2, dlg 21 and lgl 22, in the polarity-associated/Cul4-DDB1
n2:mentions: n3:7262460

Subject Item: _:vb66078376
rdf:type: n2:Context
rdf:value: In addition to Minute, many other mutations have been shown to induce a loser status against WT cells, such as mutations in the oncogene myc >>20<<, in the polarity genes scribble 2, dlg 21 and lgl 22, in the polarity-associated/Cul4-DDB1 complex component mahjong (mahj)12 and in genes associated with many signalling pathways such as BMP8, 23, JAK/STAT24, Wingless6, 25 and EGF26.
n2:mentions: n3:10499795

Subject Item: _:vb66078377
rdf:type: n2:Context
rdf:value: In addition to Minute, many other mutations have been shown to induce a loser status against WT cells, such as mutations in the oncogene myc 20, in the polarity genes scribble >>2<<, dlg 21 and lgl 22, in the polarity-associated/Cul4-DDB1 complex component mahjong (mahj)12 and in genes associated with many signalling pathways such as BMP8, 23, JAK/STAT24, Wingless6, 25 and EGF26.
n2:mentions: n3:14592975

Subject Item: _:vb66078378
rdf:type: n2:Context
rdf:value: In addition to Minute, many other mutations have been shown to induce a loser status against WT cells, such as mutations in the oncogene myc 20, in the polarity genes scribble 2, dlg >>21<< and lgl 22, in the polarity-associated/Cul4-DDB1 complex component mahjong (mahj)12 and in genes associated with many signalling pathways such as BMP8, 23, JAK/STAT24, Wingless6, 25 and EGF26.
n2:mentions: n3:21397843

Subject Item: _:vb66078379
rdf:type: n2:Context
rdf:value: In addition to Minute, many other mutations have been shown to induce a loser status against WT cells, such as mutations in the oncogene myc 20, in the polarity genes scribble 2, dlg 21 and lgl >>22<<, in the polarity-associated/Cul4-DDB1 complex component mahjong (mahj)12 and in genes associated with many signalling pathways such as BMP8, 23, JAK/STAT24, Wingless6, 25 and EGF26.
n2:mentions: n3:16753569

Subject Item: _:vb66078380
rdf:type: n2:Context
rdf:value: mutations have been shown to induce a loser status against WT cells, such as mutations in the oncogene myc 20, in the polarity genes scribble 2, dlg 21 and lgl 22, in the polarity-associated/Cul4-DDB1 complex component mahjong (mahj)>>12<< and in genes associated with many signalling pathways such as BMP8, 23, JAK/STAT24, Wingless6, 25 and EGF26.
n2:mentions: n3:20644714

Subject Item: _:vb66078381
rdf:type: n2:Context
rdf:value: such as mutations in the oncogene myc 20, in the polarity genes scribble 2, dlg 21 and lgl 22, in the polarity-associated/Cul4-DDB1 complex component mahjong (mahj)12 and in genes associated with many signalling pathways such as BMP>>8<<, 23, JAK/STAT24, Wingless6, 25 and EGF26.
n2:mentions: n3:23867226

Subject Item: _:vb66078382
rdf:type: n2:Context
rdf:value: such as mutations in the oncogene myc 20, in the polarity genes scribble 2, dlg 21 and lgl 22, in the polarity-associated/Cul4-DDB1 complex component mahjong (mahj)12 and in genes associated with many signalling pathways such as BMP8, >>23<<, JAK/STAT24, Wingless6, 25 and EGF26.
n2:mentions: n3:11961558

Subject Item: _:vb66078383
rdf:type: n2:Context
rdf:value: in the oncogene myc 20, in the polarity genes scribble 2, dlg 21 and lgl 22, in the polarity-associated/Cul4-DDB1 complex component mahjong (mahj)12 and in genes associated with many signalling pathways such as BMP8, 23, JAK/STAT>>24<<, Wingless6, 25 and EGF26.
n2:mentions: n3:22992954

Subject Item: _:vb66078384
rdf:type: n2:Context
rdf:value: the oncogene myc 20, in the polarity genes scribble 2, dlg 21 and lgl 22, in the polarity-associated/Cul4-DDB1 complex component mahjong (mahj)12 and in genes associated with many signalling pathways such as BMP8, 23, JAK/STAT24, Wingless>>6<<, 25 and EGF26.
n2:mentions: n3:26853366

Subject Item: _:vb66078385
rdf:type: n2:Context
rdf:value: oncogene myc 20, in the polarity genes scribble 2, dlg 21 and lgl 22, in the polarity-associated/Cul4-DDB1 complex component mahjong (mahj)12 and in genes associated with many signalling pathways such as BMP8, 23, JAK/STAT24, Wingless6, >>25<< and EGF26.
n2:mentions: n3:21839923

Subject Item: _:vb66078386
rdf:type: n2:Context
rdf:value: 20, in the polarity genes scribble 2, dlg 21 and lgl 22, in the polarity-associated/Cul4-DDB1 complex component mahjong (mahj)12 and in genes associated with many signalling pathways such as BMP8, 23, JAK/STAT24, Wingless6, 25 and EGF>>26<<.
n2:mentions: n3:26853367

Subject Item: _:vb66078387
rdf:type: n2:Context
rdf:value: architecture (like mutations in polarity genes) or cell-fate specification (e.g., mutations in BMP, JAK/STAT and Wingless components) and cells harbouring some of these defects show signs of stress, such as activation of the JNK pathway>>27<<. It is therefore likely that cell competition prevents the accumulation of stressed or mis-specified cells, which could compromise tissue robustness/health or contribute to developmental defects.
n2:mentions: n3:22035869

Subject Item: _:vb66078388
rdf:type: n2:Context
rdf:value: First, loser cells commonly exhibit slower proliferation rates than their winner counterparts and this passively contributes to expansion of the winner cell population>>1<<, 19. Secondly, it has been reported that during cell competition winner cells further increase their proliferation rates over their already faster baseline5, 28–31. It is unclear how that is elicited; however, it has been proposed to be a
n2:mentions: n3:1116643

Subject Item: _:vb66078389
rdf:type: n2:Context
rdf:value: First, loser cells commonly exhibit slower proliferation rates than their winner counterparts and this passively contributes to expansion of the winner cell population1, >>19<<. Secondly, it has been reported that during cell competition winner cells further increase their proliferation rates over their already faster baseline5, 28–31. It is unclear how that is elicited; however, it has been proposed to be a
n2:mentions: n3:7262460

Subject Item: _:vb66078390
rdf:type: n2:Context
rdf:value: Secondly, it has been reported that during cell competition winner cells further increase their proliferation rates over their already faster baseline>>5<<, 28–31. It is unclear how that is elicited; however, it has been proposed to be a consequence of winner/loser recognition or simply a compensatory mechanism triggered by loser cell death28–34. The third and most striking aspect of cell
n2:mentions: n3:26212135

Subject Item: _:vb66078391
rdf:type: n2:Context
rdf:value: Secondly, it has been reported that during cell competition winner cells further increase their proliferation rates over their already faster baseline5, >>28<<–31. It is unclear how that is elicited; however, it has been proposed to be a consequence of winner/loser recognition or simply a compensatory mechanism triggered by loser cell death28–34. The third and most striking aspect of cell
n2:mentions: n3:17574031 n3:15066286 n3:15066287 n3:18000039

Subject Item: _:vb66078392
rdf:type: n2:Context
rdf:value: It is unclear how that is elicited; however, it has been proposed to be a consequence of winner/loser recognition or simply a compensatory mechanism triggered by loser cell death>>28<<–34. The third and most striking aspect of cell competition is that loser cells are eliminated in the presence of their fitter neighbours1, 19, mostly (but not exclusively) via induction of apoptosis5, 23, 31, 35. Collectively, the
n2:mentions: n3:22438309 n3:17574031 n3:15066286 n3:15066287 n3:18000039 n3:20627080 n3:23509066

Subject Item: _:vb66078393
rdf:type: n2:Context
rdf:value: The third and most striking aspect of cell competition is that loser cells are eliminated in the presence of their fitter neighbours>>1<<, 19, mostly (but not exclusively) via induction of apoptosis5, 23, 31, 35.
n2:mentions: n3:1116643

Subject Item: _:vb66078394
rdf:type: n2:Context
rdf:value: The third and most striking aspect of cell competition is that loser cells are eliminated in the presence of their fitter neighbours1, >>19<<, mostly (but not exclusively) via induction of apoptosis5, 23, 31, 35.
n2:mentions: n3:7262460

Subject Item: _:vb66078395
rdf:type: n2:Context
rdf:value: The third and most striking aspect of cell competition is that loser cells are eliminated in the presence of their fitter neighbours1, 19, mostly (but not exclusively) via induction of apoptosis>>5<<, 23, 31, 35.
n2:mentions: n3:26212135

Subject Item: _:vb66078396
rdf:type: n2:Context
rdf:value: The third and most striking aspect of cell competition is that loser cells are eliminated in the presence of their fitter neighbours1, 19, mostly (but not exclusively) via induction of apoptosis5, >>23<<, 31, 35. Collectively, the combination of these three processes, results in cell competition and in the effective colonisation of tissues by winners at the expense of losers. Several molecules, such as Flower32, Azot36, the Toll/IMD
n2:mentions: n3:11961558

Subject Item: _:vb66078397
rdf:type: n2:Context
rdf:value: The third and most striking aspect of cell competition is that loser cells are eliminated in the presence of their fitter neighbours1, 19, mostly (but not exclusively) via induction of apoptosis5, 23, >>31<<, 35. Collectively, the combination of these three processes, results in cell competition and in the effective colonisation of tissues by winners at the expense of losers. Several molecules, such as Flower32, Azot36, the Toll/IMD
n2:mentions: n3:17574031

Subject Item: _:vb66078398
rdf:type: n2:Context
rdf:value: The third and most striking aspect of cell competition is that loser cells are eliminated in the presence of their fitter neighbours1, 19, mostly (but not exclusively) via induction of apoptosis5, 23, 31, >>35<<. Collectively, the combination of these three processes, results in cell competition and in the effective colonisation of tissues by winners at the expense of losers. Several molecules, such as Flower32, Azot36, the Toll/IMD pathway37,
n2:mentions: n3:22250205

Subject Item: _:vb66078399
rdf:type: n2:Context
rdf:value: Several molecules, such as Flower>>32<<, Azot36, the Toll/IMD pathway37, and the Sas/PTP10D ligand-receptor complex38 have been implicated in triggering the apoptosis of losers.
n2:mentions: n3:20627080

Subject Item: _:vb66078400
rdf:type: n2:Context
rdf:value: Several molecules, such as Flower32, Azot>>36<<, the Toll/IMD pathway37, and the Sas/PTP10D ligand-receptor complex38 have been implicated in triggering the apoptosis of losers.
n2:mentions: n3:25601460

Subject Item: _:vb66078401
rdf:type: n2:Context
rdf:value: Several molecules, such as Flower32, Azot36, the Toll/IMD pathway>>37<<, and the Sas/PTP10D ligand-receptor complex38 have been implicated in triggering the apoptosis of losers.
n2:mentions: n3:25477468

Subject Item: _:vb66078402
rdf:type: n2:Context
rdf:value: Several molecules, such as Flower32, Azot36, the Toll/IMD pathway37, and the Sas/PTP10D ligand-receptor complex>>38<< have been implicated in triggering the apoptosis of losers.
n2:mentions: n3:28092921

Subject Item: _:vb66078403
rdf:type: n5:Section
dc:title: results
n5:contains: _:vb66078440 _:vb66078441 _:vb66078442 _:vb66078443 _:vb66078444 _:vb66078445 _:vb66078446 _:vb66078447 _:vb66078432 _:vb66078433 _:vb66078434 _:vb66078435 _:vb66078436 _:vb66078437 _:vb66078438 _:vb66078439 _:vb66078456 _:vb66078457 _:vb66078458 _:vb66078448 _:vb66078449 _:vb66078450 _:vb66078451 _:vb66078452 _:vb66078453 _:vb66078454 _:vb66078455 _:vb66078408 _:vb66078409 _:vb66078410 _:vb66078411 _:vb66078412 _:vb66078413 _:vb66078414 _:vb66078415 _:vb66078404 _:vb66078405 _:vb66078406 _:vb66078407 _:vb66078424 _:vb66078425 _:vb66078426 _:vb66078427 _:vb66078428 _:vb66078429 _:vb66078430 _:vb66078431 _:vb66078416 _:vb66078417 _:vb66078418 _:vb66078419 _:vb66078420 _:vb66078421 _:vb66078422 _:vb66078423

Subject Item: _:vb66078404
rdf:type: n2:Context
rdf:value: Both alleles are mutations of the Minute gene M(3)95A and confer a loser status>>18<<, 39 (Supplementary Fig.
n2:mentions: n3:17927810

Subject Item: _:vb66078405
rdf:type: n2:Context
rdf:value: Both alleles are mutations of the Minute gene M(3)95A and confer a loser status18, >>39<< (Supplementary Fig.
n2:mentions: n3:25613379

Subject Item: _:vb66078406
rdf:type: n2:Context
rdf:value: To this aim, we compared the RpS3 +/− mutant transcriptomes to those of two additional mutants: RpS15 ribosomal gene mutants (M(2)53), which exhibits the Minute phenotype>>18<< but do not behave as losers against WT cells (Supplementary Fig.
n2:mentions: n3:17927810

Subject Item: _:vb66078407
rdf:type: n2:Context
rdf:value: 1k, l); and mutants in mahj, a gene that is functionally unrelated to ribosomal genes (mahj is an interactor of polarity genes and a component of a cullin ubiquitin ligase complex>>12<<, 40), but whose mutation nevertheless confers a loser status against WT cells12 (Fig.
n2:mentions: n3:20644714

Subject Item: _:vb66078408
rdf:type: n2:Context
rdf:value: 1k, l); and mutants in mahj, a gene that is functionally unrelated to ribosomal genes (mahj is an interactor of polarity genes and a component of a cullin ubiquitin ligase complex12, >>40<<), but whose mutation nevertheless confers a loser status against WT cells12 (Fig.
n2:mentions: n3:17314515

Subject Item: _:vb66078409
rdf:type: n2:Context
rdf:value: mahj, a gene that is functionally unrelated to ribosomal genes (mahj is an interactor of polarity genes and a component of a cullin ubiquitin ligase complex12, 40), but whose mutation nevertheless confers a loser status against WT cells>>12<< (Fig. 1a). Interestingly, there was little overlap between loser RpS3 +/− and non-loser RpS15 +/− cells (Fig.
n2:mentions: n3:20644714

Subject Item: _:vb66078410
rdf:type: n2:Context
rdf:value: This served as a proof of principle of the validity of our approach, as the Toll pathway has been shown to be activated downstream of cell competition and to lead to loser cells apoptosis>>37<<. Our data suggest that the Toll pathway might already be affected in prospective loser cells before cell competition.
n2:mentions: n3:25477468

Subject Item: _:vb66078411
rdf:type: n2:Context
rdf:value: Since the DDR is often associated with p53 activation, we cross-compared our DDR signature genes with previously identified p53 targets in Drosophila that are upregulated following DNA damage>>41<<, 42. Indeed, we found that 29 of our DDR-related genes were also proposed p53 targets (Supplementary Fig. 1o, p). This suggests that the p53 pathway is activated in prospective losers. Interestingly, however, p53 activation in Minute
n2:mentions: n3:17310982

Subject Item: _:vb66078412
rdf:type: n2:Context
rdf:value: Since the DDR is often associated with p53 activation, we cross-compared our DDR signature genes with previously identified p53 targets in Drosophila that are upregulated following DNA damage41, >>42<<. Indeed, we found that 29 of our DDR-related genes were also proposed p53 targets (Supplementary Fig. 1o, p). This suggests that the p53 pathway is activated in prospective losers. Interestingly, however, p53 activation in Minute cells
n2:mentions: n3:22666323

Subject Item: _:vb66078413
rdf:type: n2:Context
rdf:value: Interestingly, however, p53 activation in Minute cells has been shown not to be required for their autonomous cell survival or for their elimination during competition>>39<<.
n2:mentions: n3:25613379

Subject Item: _:vb66078414
rdf:type: n2:Context
rdf:value: JNK (Basket (Bsk) in Drosophila) is a major stress response factor and an important regulator of cell growth and death in many Drosophila tissues>>43<<–45. JNK signalling has also been implicated in multiple cell competition systems, such as scribble 2, mahj 12, 27, myc 28, APC 6 and Minute competition5, 23, where it has been proposed to play a role in the late stage induction of cell
n2:mentions: n3:16079158 n3:15469838 n3:15766749

Subject Item: _:vb66078415
rdf:type: n2:Context
rdf:value: JNK signalling has also been implicated in multiple cell competition systems, such as scribble >>2<<, mahj 12, 27, myc 28, APC 6 and Minute competition5, 23, where it has been proposed to play a role in the late stage induction of cell death, although this is controversial in the case of Minute and myc-induced cell competition29, 46.
n2:mentions: n3:14592975

Subject Item: _:vb66078416
rdf:type: n2:Context
rdf:value: JNK signalling has also been implicated in multiple cell competition systems, such as scribble 2, mahj >>12<<, 27, myc 28, APC 6 and Minute competition5, 23, where it has been proposed to play a role in the late stage induction of cell death, although this is controversial in the case of Minute and myc-induced cell competition29, 46.
n2:mentions: n3:20644714

Subject Item: _:vb66078417
rdf:type: n2:Context
rdf:value: JNK signalling has also been implicated in multiple cell competition systems, such as scribble 2, mahj 12, >>27<<, myc 28, APC 6 and Minute competition5, 23, where it has been proposed to play a role in the late stage induction of cell death, although this is controversial in the case of Minute and myc-induced cell competition29, 46.
n2:mentions: n3:22035869

Subject Item: _:vb66078418
rdf:type: n2:Context
rdf:value: JNK signalling has also been implicated in multiple cell competition systems, such as scribble 2, mahj 12, 27, myc >>28<<, APC 6 and Minute competition5, 23, where it has been proposed to play a role in the late stage induction of cell death, although this is controversial in the case of Minute and myc-induced cell competition29, 46.
n2:mentions: n3:15066287

Subject Item: _:vb66078419
rdf:type: n2:Context
rdf:value: JNK signalling has also been implicated in multiple cell competition systems, such as scribble 2, mahj 12, 27, myc 28, APC >>6<< and Minute competition5, 23, where it has been proposed to play a role in the late stage induction of cell death, although this is controversial in the case of Minute and myc-induced cell competition29, 46.
n2:mentions: n3:26853366

Subject Item: _:vb66078420
rdf:type: n2:Context
rdf:value: JNK signalling has also been implicated in multiple cell competition systems, such as scribble 2, mahj 12, 27, myc 28, APC 6 and Minute competition>>5<<, 23, where it has been proposed to play a role in the late stage induction of cell death, although this is controversial in the case of Minute and myc-induced cell competition29, 46.
n2:mentions: n3:26212135

Subject Item: _:vb66078421
rdf:type: n2:Context
rdf:value: JNK signalling has also been implicated in multiple cell competition systems, such as scribble 2, mahj 12, 27, myc 28, APC 6 and Minute competition5, >>23<<, where it has been proposed to play a role in the late stage induction of cell death, although this is controversial in the case of Minute and myc-induced cell competition29, 46.
n2:mentions: n3:11961558

Subject Item: _:vb66078422
rdf:type: n2:Context
rdf:value: 2, mahj 12, 27, myc 28, APC 6 and Minute competition5, 23, where it has been proposed to play a role in the late stage induction of cell death, although this is controversial in the case of Minute and myc-induced cell competition>>29<<, 46. Our RNAseq data indicates that both Minute and mahj −/− cells in their naive state upregulate the JNK pathway (as both JNK activators, such as Gadd45 and JNK target genes, such as scarface 47 and reaper 45 are upregulated (Fig.
n2:mentions: n3:15066286

Subject Item: _:vb66078423
rdf:type: n2:Context
rdf:value: 2, mahj 12, 27, myc 28, APC 6 and Minute competition5, 23, where it has been proposed to play a role in the late stage induction of cell death, although this is controversial in the case of Minute and myc-induced cell competition29, >>46<<. Our RNAseq data indicates that both Minute and mahj −/− cells in their naive state upregulate the JNK pathway (as both JNK activators, such as Gadd45 and JNK target genes, such as scarface 47 and reaper 45 are upregulated (Fig.
n2:mentions: n3:17110495

Subject Item: _:vb66078424
rdf:type: n2:Context
rdf:value: Our RNAseq data indicates that both Minute and mahj −/− cells in their naive state upregulate the JNK pathway (as both JNK activators, such as Gadd45 and JNK target genes, such as scarface >>47<< and reaper 45 are upregulated (Fig.
n2:mentions: n3:20530545

Subject Item: _:vb66078425
rdf:type: n2:Context
rdf:value: Our RNAseq data indicates that both Minute and mahj −/− cells in their naive state upregulate the JNK pathway (as both JNK activators, such as Gadd45 and JNK target genes, such as scarface 47 and reaper >>45<< are upregulated (Fig.
n2:mentions: n3:16079158

Subject Item: _:vb66078426
rdf:type: n2:Context
rdf:value: 2a)), in agreement with earlier reports>>27<<. In addition we found that RpS3 +/− cells show strong activation of the JNK reporter TRE-dsRED48 (Fig.
n2:mentions: n3:22035869

Subject Item: _:vb66078427
rdf:type: n2:Context
rdf:value: In addition we found that RpS3 +/− cells show strong activation of the JNK reporter TRE-dsRED>>48<< (Fig. 2b,d,e) and of active phosphorylated-JNK6 (pJNK; Supplementary Fig. 2a, c, d) compared to WT cells, whereas naive RpS15 +/− cells, which do not behave as losers, show a markedly lower level of reporter activation (Fig. 2b,c,e and
n2:mentions: n3:22509270

Subject Item: _:vb66078428
rdf:type: n2:Context
rdf:value: 2b,d,e) and of active phosphorylated-JNK>>6<< (pJNK; Supplementary Fig. 2a, c, d) compared to WT cells, whereas naive RpS15 +/− cells, which do not behave as losers, show a markedly lower level of reporter activation (Fig.
n2:mentions: n3:26853366

Subject Item: _:vb66078429
rdf:type: n2:Context
rdf:value: To address this, we inhibited JNK signalling specifically in loser RpS3 +/− cells during cell competition, by overexpressing the JNK inhibitor puckered (puc) >>45<<, 49. JNK inhibition reduced competition-induced cell death, as expected23 (Supplementary Fig. 2e–g). However, we also noted a striking increase in the overall ability of RpS3 +/− cells to colonise the tissue (Fig. 2f, g), consistent with
n2:mentions: n3:16079158

Subject Item: _:vb66078430
rdf:type: n2:Context
rdf:value: To address this, we inhibited JNK signalling specifically in loser RpS3 +/− cells during cell competition, by overexpressing the JNK inhibitor puckered (puc) 45, >>49<<. JNK inhibition reduced competition-induced cell death, as expected23 (Supplementary Fig. 2e–g). However, we also noted a striking increase in the overall ability of RpS3 +/− cells to colonise the tissue (Fig. 2f, g), consistent with the
n2:mentions: n3:9472024

Subject Item: _:vb66078431
rdf:type: n2:Context
rdf:value: JNK inhibition reduced competition-induced cell death, as expected>>23<< (Supplementary Fig.
n2:mentions: n3:11961558

Subject Item: _:vb66078432
rdf:type: n2:Context
rdf:value: JNK overactivation leads to autonomous cell death>>45<<; however, after carefully optimising JNK activation levels (by partial silencing of the JNK inhibitor puc using tub-Gal80 TS, see Supplementary Table 1), we obtained large clones with active JNK, so as to assess whether they would behave
n2:mentions: n3:16079158

Subject Item: _:vb66078433
rdf:type: n2:Context
rdf:value: These clones displayed some residual apoptosis, however unlike during Minute cell competition, where cell death is observed within 1–2 cell diameters of the clone boundary>>31<< (Supplementary Fig.
n2:mentions: n3:17574031

Subject Item: _:vb66078434
rdf:type: n2:Context
rdf:value: We next wondered whether the increase in clone size was due to the anti-apoptotic effect of JNK inhibition, which could inhibit background-level cell death in Minute cells>>50<<, leading to bigger clone sizes.
n2:mentions: n3:16291791

Subject Item: _:vb66078435
rdf:type: n2:Context
rdf:value: The JAK/STAT pathway is a cytokine signalling pathway involved in the proliferative, immune and inflammatory responses51, >>52<<. Specifically in Drosophila imaginal discs, the pathway is required for developmental patterning53, 54 and to promote proliferation under normal conditions and during regeneration52, 55.
n2:mentions: n3:24069565

Subject Item: _:vb66078436
rdf:type: n2:Context
rdf:value: Specifically in Drosophila imaginal discs, the pathway is required for developmental patterning>>53<<, 54 and to promote proliferation under normal conditions and during regeneration52, 55.
n2:mentions: n3:23978534

Subject Item: _:vb66078437
rdf:type: n2:Context
rdf:value: Specifically in Drosophila imaginal discs, the pathway is required for developmental patterning53, >>54<< and to promote proliferation under normal conditions and during regeneration52, 55.
n2:mentions: n3:17079268

Subject Item: _:vb66078438
rdf:type: n2:Context
rdf:value: Specifically in Drosophila imaginal discs, the pathway is required for developmental patterning53, 54 and to promote proliferation under normal conditions and during regeneration>>52<<, 55. Our RNAseq data show that both RpS3 +/− and mahj −/− cells upregulate the JAK/STAT targets Socs36E and chinmo as well as all three ligands of the pathway—the cytokines unpaired 1, 2 and 3 (upd, upd2, upd3)56–58 (Fig. 4a), suggesting
n2:mentions: n3:24069565

Subject Item: _:vb66078439
rdf:type: n2:Context
rdf:value: Specifically in Drosophila imaginal discs, the pathway is required for developmental patterning53, 54 and to promote proliferation under normal conditions and during regeneration52, >>55<<. Our RNAseq data show that both RpS3 +/− and mahj −/− cells upregulate the JAK/STAT targets Socs36E and chinmo as well as all three ligands of the pathway—the cytokines unpaired 1, 2 and 3 (upd, upd2, upd3)56–58 (Fig. 4a), suggesting
n2:mentions: n3:25902518

Subject Item: _:vb66078440
rdf:type: n2:Context
rdf:value: Our RNAseq data show that both RpS3 +/− and mahj −/− cells upregulate the JAK/STAT targets Socs36E and chinmo as well as all three ligands of the pathway—the cytokines unpaired 1, 2 and 3 (upd, upd2, upd3)>>56<<–58 (Fig. 4a), suggesting pathway activation. We first validated these findings using an in vivo fluorescent reporter of STAT activity (10xSTAT-GFP59). Indeed we found that RpS3 +/− cells display reporter activation compared to WT cells
n2:mentions: n3:9784499 n3:16277982 n3:12967563

Subject Item: _:vb66078441
rdf:type: n2:Context
rdf:value: We first validated these findings using an in vivo fluorescent reporter of STAT activity (10xSTAT-GFP>>59<<). Indeed we found that RpS3 +/− cells display reporter activation compared to WT cells (Figs. 4b, c) and upregulate upd3 expression as detected by in situ (Supplementary Fig. 4a, b), by upd3-Gal4, UAS-GFP expression (Fig. 4d, e and
n2:mentions: n3:17008134

Subject Item: _:vb66078442
rdf:type: n2:Context
rdf:value: We next asked whether JNK signalling, which has been shown to activate Upd ligands in this and other tissues>>60<<–62, was responsible for the production of Upd ligands in RpS3 +/− wing discs.
n2:mentions: n3:20072127 n3:23023132

Subject Item: _:vb66078443
rdf:type: n2:Context
rdf:value: Notably JAK-STAT inhibition in the P compartment, by expression of a dominant-negative version of the receptor Dome (DomeΔCyt)>>63<< (whose activity we confirmed by monitoring the activity of the 10xSTAT-GFP reporter; Supplementary Fig.
n2:mentions: n3:11696329

Subject Item: _:vb66078444
rdf:type: n2:Context
rdf:value: It has long been known that during cell competition winner cells proliferate faster than they would normally do on their own>>5<<, 28–31. This has mostly been attributed to winner–loser recognition signals or to apoptosis-induced proliferation32–34.
n2:mentions: n3:26212135

Subject Item: _:vb66078445
rdf:type: n2:Context
rdf:value: It has long been known that during cell competition winner cells proliferate faster than they would normally do on their own5, >>28<<–31. This has mostly been attributed to winner–loser recognition signals or to apoptosis-induced proliferation32–34.
n2:mentions: n3:18000039 n3:15066286 n3:15066287 n3:17574031

Subject Item: _:vb66078446
rdf:type: n2:Context
rdf:value: This has mostly been attributed to winner–loser recognition signals or to apoptosis-induced proliferation>>32<<–34. However, Upds are soluble proteins capable of long-range signalling and have been reported to cause non-autonomous overgrowth phenotypes61, 62. In addition we recently showed that in the adult Drosophila midgut Upd ligands produced by
n2:mentions: n3:20627080 n3:23509066 n3:22438309

Subject Item: _:vb66078447
rdf:type: n2:Context
rdf:value: However, Upds are soluble proteins capable of long-range signalling and have been reported to cause non-autonomous overgrowth phenotypes>>61<<, 62. In addition we recently showed that in the adult Drosophila midgut Upd ligands produced by RpS3 +/− cells promote the proliferation of WT cells during cell competition5. This suggested that their production from RpS3 +/− wing disc
n2:mentions: n3:23023132

Subject Item: _:vb66078448
rdf:type: n2:Context
rdf:value: However, Upds are soluble proteins capable of long-range signalling and have been reported to cause non-autonomous overgrowth phenotypes61, >>62<<. In addition we recently showed that in the adult Drosophila midgut Upd ligands produced by RpS3 +/− cells promote the proliferation of WT cells during cell competition5. This suggested that their production from RpS3 +/− wing disc cells
n2:mentions: n3:20072127

Subject Item: _:vb66078449
rdf:type: n2:Context
rdf:value: In addition we recently showed that in the adult Drosophila midgut Upd ligands produced by RpS3 +/− cells promote the proliferation of WT cells during cell competition>>5<<. This suggested that their production from RpS3 +/− wing disc cells could have a similar effect on winner cell proliferation in this tissue. Indeed, we found that just removing one copy of the pathway receptor Dome was sufficient to
n2:mentions: n3:26212135

Subject Item: _:vb66078450
rdf:type: n2:Context
rdf:value: These include multiple known target genes of the mammalian transcription factor Nrf>>264<< (CncC in Drosophila 65), although neither the CncC gene itself nor the canonical inhibitor of the pathway Keap1 are transcriptionally affected (Supplementary Data 1).
n2:mentions: n3:21365312

Subject Item: _:vb66078451
rdf:type: n2:Context
rdf:value: These include multiple known target genes of the mammalian transcription factor Nrf264 (CncC in Drosophila >>65<<), although neither the CncC gene itself nor the canonical inhibitor of the pathway Keap1 are transcriptionally affected (Supplementary Data 1).
n2:mentions: n3:18194654

Subject Item: _:vb66078452
rdf:type: n2:Context
rdf:value: regulator of the oxidative stress response and is involved in the adaptation to oxidative and chemical stress through upregulation of a number of genes with anti-oxidant function or involved in the removal of harmful oxidation products>>64<<. Specifically, we found that prospective loser cells show upregulation of genes involved in glutathione synthesis (glutamate-cysteine ligase catalytic subunit—Gclc), glutathione conjugation to xenobiotics (glutathione
n2:mentions: n3:21365312

Subject Item: _:vb66078453
rdf:type: n2:Context
rdf:value: To confirm activation of the Nrf2 pathway in loser cells, we used a fluorescent transcriptional reporter of Nrf2—GstD1-GFP>>65<<. In line with our RNAseq data, both RpS3 +/− (Fig. 5c, d and Supplementary Fig. 5a–c) and mahj RNAi (Fig. 5e, f) cells exhibited higher levels of reporter expression compared to WT cells, both before and during cell competition,
n2:mentions: n3:18194654

Subject Item: _:vb66078454
rdf:type: n2:Context
rdf:value: Reactive oxygen species (ROS), are powerful activators of Nrf2 and have been shown to be produced under some metabolic imbalance conditions>>61<<. However, RpS3 +/− cells showed only a negligible increase in dihydroethidium (DHE) staining (Supplementary Fig. 5d, e) and a decrease in CM-H2DCFDA staining (Supplementary Fig. 5f, g), two widely used fluorescent dyes sensitive to
n2:mentions: n3:23023132

Subject Item: _:vb66078455
rdf:type: n2:Context
rdf:value: 5f, g), two widely used fluorescent dyes sensitive to different types of ROS>>61<<. Given that prospective loser cells display the upregulation of several enzymes involved in glutathione synthesis or utilisation (Fig.
n2:mentions: n3:23023132

Subject Item: _:vb66078456
rdf:type: n2:Context
rdf:value: 5a) and given that free reduced glutathione is the main cytosolic anti-oxidant and regulator of the cytosolic redox state>>66<<, we wondered whether the oxidative stress response might instead be triggered by low cytosolic levels of reduced glutathione.
n2:mentions: n3:18796312

Subject Item: _:vb66078457
rdf:type: n2:Context
rdf:value: Nrf2 is generally considered a stress adaptation factor and typically serves a pro-survival role>>64<<, 65. Indeed we found that knockdown of Nrf2 by Nrf2 RNAi causes increased cell death in RpS3 +/− cells, but not in WT cells (Fig.
n2:mentions: n3:21365312

Subject Item: _:vb66078458
rdf:type: n2:Context
rdf:value: Nrf2 is generally considered a stress adaptation factor and typically serves a pro-survival role64, >>65<<. Indeed we found that knockdown of Nrf2 by Nrf2 RNAi causes increased cell death in RpS3 +/− cells, but not in WT cells (Fig.
n2:mentions: n3:18194654

Subject Item: _:vb66078459
rdf:type: n5:Section
dc:title: methods
n5:contains: _:vb66078464 _:vb66078465 _:vb66078466 _:vb66078467 _:vb66078468 _:vb66078460 _:vb66078461 _:vb66078462 _:vb66078463

Subject Item: _:vb66078460
rdf:type: n2:Context
rdf:value: The following Drosophila stocks were used: RpS3[Plac92] (BL5627), RpS3*(BL5699), M(2)53 >>1<< (BL5698), FRT42D mahj 12, TRE-16 48, UAS-puc-RNAi (B.
n2:mentions: n3:1116643

Subject Item: _:vb66078461
rdf:type: n2:Context
rdf:value: The following Drosophila stocks were used: RpS3[Plac92] (BL5627), RpS3*(BL5699), M(2)53 1 (BL5698), FRT42D mahj >>12<<, TRE-16 48, UAS-puc-RNAi (B.
n2:mentions: n3:20644714

Subject Item: _:vb66078462
rdf:type: n2:Context
rdf:value: The following Drosophila stocks were used: RpS3[Plac92] (BL5627), RpS3*(BL5699), M(2)53 1 (BL5698), FRT42D mahj 12, TRE-16 >>48<<, UAS-puc-RNAi (B.
n2:mentions: n3:22509270

Subject Item: _:vb66078463
rdf:type: n2:Context
rdf:value: Perrimon), 10xSTAT-GFP >>59<<, UAS-Dome ΔCyt 63, Dome g0218 (BL11953), GstD1-GFP65, UAS-mahj-RNAi (BL34912), UAS-Nrf2-RNAi65, UAS-Nrf2 65, UAS-dIAP1 (P.
n2:mentions: n3:17008134

Subject Item: _:vb66078464
rdf:type: n2:Context
rdf:value: Perrimon), 10xSTAT-GFP 59, UAS-Dome ΔCyt >>63<<, Dome g0218 (BL11953), GstD1-GFP65, UAS-mahj-RNAi (BL34912), UAS-Nrf2-RNAi65, UAS-Nrf2 65, UAS-dIAP1 (P.
n2:mentions: n3:11696329

Subject Item: _:vb66078465
rdf:type: n2:Context
rdf:value: Perrimon), 10xSTAT-GFP 59, UAS-Dome ΔCyt 63, Dome g0218 (BL11953), GstD1-GFP>>65<<, UAS-mahj-RNAi (BL34912), UAS-Nrf2-RNAi65, UAS-Nrf2 65, UAS-dIAP1 (P.
n2:mentions: n3:18194654

Subject Item: _:vb66078466
rdf:type: n2:Context
rdf:value: Perrimon), 10xSTAT-GFP 59, UAS-Dome ΔCyt 63, Dome g0218 (BL11953), GstD1-GFP65, UAS-mahj-RNAi (BL34912), UAS-Nrf2-RNAi>>65<<, UAS-Nrf2 65, UAS-dIAP1 (P.
n2:mentions: n3:18194654

Subject Item: _:vb66078467
rdf:type: n2:Context
rdf:value: Perrimon), 10xSTAT-GFP 59, UAS-Dome ΔCyt 63, Dome g0218 (BL11953), GstD1-GFP65, UAS-mahj-RNAi (BL34912), UAS-Nrf2-RNAi65, UAS-Nrf2 >>65<<, UAS-dIAP1 (P.
n2:mentions: n3:18194654

Subject Item: _:vb66078468
rdf:type: n2:Context
rdf:value: Clone areas were measured on a medial section of the pouch region either manually or using a custom script in Fiji>>75<<. For cell death quantifications, cells that were positive for cleaved caspase-3 (by immunostaining) and within the pouch region were counted. The total number of dying cells was normalised to the respective clone area/perimeter.
n2:mentions: n3:22743772

Subject Item: _:vb66078469
rdf:type: n5:Section
dc:title: discussion
n5:contains: _:vb66078496 _:vb66078497 _:vb66078498 _:vb66078499 _:vb66078500 _:vb66078501 _:vb66078502 _:vb66078480 _:vb66078481 _:vb66078482 _:vb66078483 _:vb66078484 _:vb66078485 _:vb66078486 _:vb66078487 _:vb66078488 _:vb66078489 _:vb66078490 _:vb66078491 _:vb66078492 _:vb66078493 _:vb66078494 _:vb66078495 _:vb66078470 _:vb66078471 _:vb66078472 _:vb66078473 _:vb66078474 _:vb66078475 _:vb66078476 _:vb66078477 _:vb66078478 _:vb66078479

Subject Item: _:vb66078470
rdf:type: n2:Context
rdf:value: While it is increasingly recognised that cells can compete via multiple unrelated mechanisms>>13<<, 23–25, 36–38, 67, 68 our understanding of even the best characterised and prototypical models of cell competition, such as Minute cell competition, is still rather fragmented.
n2:mentions: n3:27109213

Subject Item: _:vb66078471
rdf:type: n2:Context
rdf:value: While it is increasingly recognised that cells can compete via multiple unrelated mechanisms13, >>23<<–25, 36–38, 67, 68 our understanding of even the best characterised and prototypical models of cell competition, such as Minute cell competition, is still rather fragmented.
n2:mentions: n3:21839923 n3:11961558 n3:22992954

Subject Item: _:vb66078472
rdf:type: n2:Context
rdf:value: While it is increasingly recognised that cells can compete via multiple unrelated mechanisms13, 23–25, >>36<<–38, 67, 68 our understanding of even the best characterised and prototypical models of cell competition, such as Minute cell competition, is still rather fragmented.
n2:mentions: n3:25601460 n3:25477468 n3:28092921

Subject Item: _:vb66078473
rdf:type: n2:Context
rdf:value: Constitutive JNK pathway activation in loser cells has been previously reported>>27<<. However, it was thought that JNK signalling simply provides a pro-apoptotic signal during competition.
n2:mentions: n3:22035869

Subject Item: _:vb66078474
rdf:type: n2:Context
rdf:value: Several reports have indicated that winner cells enhance their proliferation in various cell competition models>>5<<, 6, 8, 28–31, including Minute competition5, 29, 31. However, it has more recently been reported that during Minute cell competition WT cells grow at their normal cell-autonomous rates69.
n2:mentions: n3:26212135

Subject Item: _:vb66078475
rdf:type: n2:Context
rdf:value: Several reports have indicated that winner cells enhance their proliferation in various cell competition models5, >>6<<, 8, 28–31, including Minute competition5, 29, 31. However, it has more recently been reported that during Minute cell competition WT cells grow at their normal cell-autonomous rates69.
n2:mentions: n3:26853366

Subject Item: _:vb66078476
rdf:type: n2:Context
rdf:value: Several reports have indicated that winner cells enhance their proliferation in various cell competition models5, 6, >>8<<, 28–31, including Minute competition5, 29, 31. However, it has more recently been reported that during Minute cell competition WT cells grow at their normal cell-autonomous rates69.
n2:mentions: n3:23867226

Subject Item: _:vb66078477
rdf:type: n2:Context
rdf:value: Several reports have indicated that winner cells enhance their proliferation in various cell competition models5, 6, 8, >>28<<–31, including Minute competition5, 29, 31. However, it has more recently been reported that during Minute cell competition WT cells grow at their normal cell-autonomous rates69.
n2:mentions: n3:17574031 n3:15066286 n3:15066287 n3:18000039

Subject Item: _:vb66078478
rdf:type: n2:Context
rdf:value: Several reports have indicated that winner cells enhance their proliferation in various cell competition models5, 6, 8, 28–31, including Minute competition>>5<<, 29, 31. However, it has more recently been reported that during Minute cell competition WT cells grow at their normal cell-autonomous rates69.
n2:mentions: n3:26212135

Subject Item: _:vb66078479
rdf:type: n2:Context
rdf:value: Several reports have indicated that winner cells enhance their proliferation in various cell competition models5, 6, 8, 28–31, including Minute competition5, >>29<<, 31. However, it has more recently been reported that during Minute cell competition WT cells grow at their normal cell-autonomous rates69.
n2:mentions: n3:15066286

Subject Item: _:vb66078480
rdf:type: n2:Context
rdf:value: Several reports have indicated that winner cells enhance their proliferation in various cell competition models5, 6, 8, 28–31, including Minute competition5, 29, >>31<<. However, it has more recently been reported that during Minute cell competition WT cells grow at their normal cell-autonomous rates69.
n2:mentions: n3:17574031

Subject Item: _:vb66078481
rdf:type: n2:Context
rdf:value: However, it has more recently been reported that during Minute cell competition WT cells grow at their normal cell-autonomous rates>>69<<. This is in apparent contradiction with our finding that during cell competition Minute cells promote the proliferation of WT cells above their intrinsic rate by stimulating JAK/STAT signalling. We think that this apparent discrepancy can
n2:mentions: n3:19855017

Subject Item: _:vb66078482
rdf:type: n2:Context
rdf:value: We think that this apparent discrepancy can be resolved, if considering the experimental design in Martin and Morata>>69<<. Their conclusion was based on the observation that clones of WT cells, allowed to grow for the same amount of time (e.g., 48 h) before they are analysed at the end of third instar, reach similar sizes irrespective of whether they were in
n2:mentions: n3:19855017

Subject Item: _:vb66078483
rdf:type: n2:Context
rdf:value: Furthermore our results are consistent with our earlier observation that in the adult posterior midgut WT clones overgrow during Minute cell competition in a JAK-STAT-dependent manner>>5<<. This might have been a peculiarity of the midgut, where JAK-STAT signalling is commonly activated as part of the gut homeostasis/repair70. Our new data indicate instead that this is a general phenomenon integral to Minute cell
n2:mentions: n3:26212135

Subject Item: _:vb66078484
rdf:type: n2:Context
rdf:value: This might have been a peculiarity of the midgut, where JAK-STAT signalling is commonly activated as part of the gut homeostasis/repair>>70<<. Our new data indicate instead that this is a general phenomenon integral to Minute cell competition.
n2:mentions: n3:19563763

Subject Item: _:vb66078485
rdf:type: n2:Context
rdf:value: Indeed, while some of the signals involved in loser cell elimination have now been identified>>23<<, 32, 36–38, 71, no signal involved in the overproliferation of fitter cells during cell competition had been found so far.
n2:mentions: n3:11961558

Subject Item: _:vb66078486
rdf:type: n2:Context
rdf:value: Indeed, while some of the signals involved in loser cell elimination have now been identified23, >>32<<, 36–38, 71, no signal involved in the overproliferation of fitter cells during cell competition had been found so far.
n2:mentions: n3:20627080

Subject Item: _:vb66078487
rdf:type: n2:Context
rdf:value: Indeed, while some of the signals involved in loser cell elimination have now been identified23, 32, >>36<<–38, 71, no signal involved in the overproliferation of fitter cells during cell competition had been found so far.
n2:mentions: n3:25601460 n3:25477468 n3:28092921

Subject Item: _:vb66078488
rdf:type: n2:Context
rdf:value: Indeed, while some of the signals involved in loser cell elimination have now been identified23, 32, 36–38, >>71<<, no signal involved in the overproliferation of fitter cells during cell competition had been found so far.
n2:mentions: n3:23108407

Subject Item: _:vb66078489
rdf:type: n2:Context
rdf:value: It has been suggested that winner cells overproliferation stems from winner/loser recognition>>32<<, 33, or from compensatory proliferative signals emanating from dying loser cells31, 34.
n2:mentions: n3:20627080

Subject Item: _:vb66078490
rdf:type: n2:Context
rdf:value: It has been suggested that winner cells overproliferation stems from winner/loser recognition32, >>33<<, or from compensatory proliferative signals emanating from dying loser cells31, 34.
n2:mentions: n3:22438309

Subject Item: _:vb66078491
rdf:type: n2:Context
rdf:value: It has been suggested that winner cells overproliferation stems from winner/loser recognition32, 33, or from compensatory proliferative signals emanating from dying loser cells>>31<<, 34. Our data instead demonstrates that, at least for Minute cell competition, the overproliferation of winner cells is not a consequence of and in fact is independent of winner/loser cell recognition and of loser cell death, since Upd-2
n2:mentions: n3:17574031

Subject Item: _:vb66078492
rdf:type: n2:Context
rdf:value: It has been suggested that winner cells overproliferation stems from winner/loser recognition32, 33, or from compensatory proliferative signals emanating from dying loser cells31, >>34<<. Our data instead demonstrates that, at least for Minute cell competition, the overproliferation of winner cells is not a consequence of and in fact is independent of winner/loser cell recognition and of loser cell death, since Upd-2 and
n2:mentions: n3:23509066

Subject Item: _:vb66078493
rdf:type: n2:Context
rdf:value: Interestingly, it has previously been shown that high STAT activity can induce the winner status>>24<<. Thus it seems counterintuitive that Minute cells, which have high stat levels (most likely as a result of autocrine signalling), are losers against WT cells with lower STAT signalling.
n2:mentions: n3:22992954

Subject Item: _:vb66078494
rdf:type: n2:Context
rdf:value: For example cells that overexpress dMyc, lose their ability to outcompete cells if they are also Minute +/− >>28<<.
n2:mentions: n3:15066287

Subject Item: _:vb66078495
rdf:type: n2:Context
rdf:value: In addition this observation might help explain the elevated cancer risk associated with patients affected by ribosomopathies>>72<<, genetic diseases caused by mutations in ribosome genes.
n2:mentions: n3:20012593

Subject Item: _:vb66078496
rdf:type: n2:Context
rdf:value: Given that inflammation plays a key role in promoting cancer>>73<< our findings that cells with ribosomal mutations activate a chronic inflammatory/pro-proliferative response could provide a molecular explanation for this predisposition.
n2:mentions: n3:26289312

Subject Item: _:vb66078497
rdf:type: n2:Context
rdf:value: Exciting recent advances point at a role for Flower, Toll and PTP10D signalling as factors involved earmarking cells as losers and/or in their elimination>>32<<, 37, 38. However what pre-existing conditions prime cells as losers and initiate cell competition is not known. Importantly, our work reveals that RpS3 +/− and mahj −/− cells share a common chronic activation of the oxidative stress
n2:mentions: n3:20627080

Subject Item: _:vb66078498
rdf:type: n2:Context
rdf:value: Exciting recent advances point at a role for Flower, Toll and PTP10D signalling as factors involved earmarking cells as losers and/or in their elimination32, >>37<<, 38. However what pre-existing conditions prime cells as losers and initiate cell competition is not known. Importantly, our work reveals that RpS3 +/− and mahj −/− cells share a common chronic activation of the oxidative stress response
n2:mentions: n3:25477468

Subject Item: _:vb66078499
rdf:type: n2:Context
rdf:value: Exciting recent advances point at a role for Flower, Toll and PTP10D signalling as factors involved earmarking cells as losers and/or in their elimination32, 37, >>38<<. However what pre-existing conditions prime cells as losers and initiate cell competition is not known. Importantly, our work reveals that RpS3 +/− and mahj −/− cells share a common chronic activation of the oxidative stress response and
n2:mentions: n3:28092921

Subject Item: _:vb66078500
rdf:type: n2:Context
rdf:value: Nrf2 canonically serves a pro-survival role, protecting cells from the negative effects of toxic/oxidising compounds>>64<<, 65. This is the case also for RpS3 +/− and mahj −/− cells, since silencing Nrf2 causes autonomous cell death in Minute cells.
n2:mentions: n3:21365312

Subject Item: _:vb66078501
rdf:type: n2:Context
rdf:value: Nrf2 canonically serves a pro-survival role, protecting cells from the negative effects of toxic/oxidising compounds64, >>65<<. This is the case also for RpS3 +/− and mahj −/− cells, since silencing Nrf2 causes autonomous cell death in Minute cells.
n2:mentions: n3:18194654

Subject Item: _:vb66078502
rdf:type: n2:Context
rdf:value: As oxidative stress is activated in a number of pathological conditions including cancer>>74<<, our findings suggest that cell competition might be common in these instances and potentially plays a role in disease prevention and progression.
n2:mentions: n3:24142871

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