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Subject Item: n2:19840402
rdf:type: n3:RelevantPaper n3:ReferencePaper n3:CitationPaper
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bibo:doi: 10.1186%2F1471-213X-9-53
n9:contains: _:vb6245527 _:vb6245533 _:vb6245538 _:vb6245502

Subject Item: _:vb6245502
rdf:type: n9:Section
dc:title: results
n9:contains: _:vb6245503 _:vb6245524 _:vb6245525 _:vb6245526 _:vb6245520 _:vb6245521 _:vb6245522 _:vb6245523 _:vb6245516 _:vb6245517 _:vb6245518 _:vb6245519 _:vb6245512 _:vb6245513 _:vb6245514 _:vb6245515 _:vb6245508 _:vb6245509 _:vb6245510 _:vb6245511 _:vb6245504 _:vb6245505 _:vb6245506 _:vb6245507

Subject Item: _:vb6245503
rdf:type: n3:Context
rdf:value: Complementation tests of the mutation with four known ras loss-of-function alleles, rasD38N [>>22<<], ras85DelB [23,22], rasΔC40b, and ras ΔC17b [24], failed to rescue ras dependent lethality.
n3:mentions: n2:1934068

Subject Item: _:vb6245504
rdf:type: n3:Context
rdf:value: Complementation tests of the mutation with four known ras loss-of-function alleles, rasD38N [22], ras85DelB [>>23<<,22], rasΔC40b, and ras ΔC17b [24], failed to rescue ras dependent lethality.
n3:mentions: n2:8384582

Subject Item: _:vb6245505
rdf:type: n3:Context
rdf:value: Complementation tests of the mutation with four known ras loss-of-function alleles, rasD38N [22], ras85DelB [23,>>22<<], rasΔC40b, and ras ΔC17b [24], failed to rescue ras dependent lethality.
n3:mentions: n2:1934068

Subject Item: _:vb6245506
rdf:type: n3:Context
rdf:value: Complementation tests of the mutation with four known ras loss-of-function alleles, rasD38N [22], ras85DelB [23,22], rasΔC40b, and ras ΔC17b [>>24<<], failed to rescue ras dependent lethality.
n3:mentions: n2:8978043

Subject Item: _:vb6245507
rdf:type: n3:Context
rdf:value: During Drosophila eye development, Ras contributes positively to the regulation of cell growth [>>25<<] and cell differentiation [26], but negatively to the regulation of apoptosis [9,10].
n3:mentions: n2:9389658

Subject Item: _:vb6245508
rdf:type: n3:Context
rdf:value: During Drosophila eye development, Ras contributes positively to the regulation of cell growth [25] and cell differentiation [>>26<<], but negatively to the regulation of apoptosis [9,10]. Such diverse biological effects are thought to be achieved through different levels of Ras activity [27].
n3:mentions: n2:1311054

Subject Item: _:vb6245509
rdf:type: n3:Context
rdf:value: During Drosophila eye development, Ras contributes positively to the regulation of cell growth [25] and cell differentiation [26], but negatively to the regulation of apoptosis [>>9<<,10]. Such diverse biological effects are thought to be achieved through different levels of Ras activity [27].
n3:mentions: n2:9814704

Subject Item: _:vb6245510
rdf:type: n3:Context
rdf:value: During Drosophila eye development, Ras contributes positively to the regulation of cell growth [25] and cell differentiation [26], but negatively to the regulation of apoptosis [9,>>10<<]. Such diverse biological effects are thought to be achieved through different levels of Ras activity [27].
n3:mentions: n2:9814703

Subject Item: _:vb6245511
rdf:type: n3:Context
rdf:value: Such diverse biological effects are thought to be achieved through different levels of Ras activity [>>27<<]. rasKP homozygous mutants have small and rough eyes (Figure 1C). To determine the developmental basis of the phenotype, we compare the growth of third instar larval eye imaginal discs of rasKP mutant and wild-type. Both were of similar
n3:mentions: n2:11290305

Subject Item: _:vb6245512
rdf:type: n3:Context
rdf:value: Neuronal differentiation in the eye discs, as revealed by anti-Elav antibody staining [>>28<<], do occur in rasKP third instar larvae (Figure 3A-C).
n3:mentions: n2:1716300

Subject Item: _:vb6245513
rdf:type: n3:Context
rdf:value: In Drosophila, Ras has been shown to promote cell survival by both down regulating hid expression and inactivating Hid protein through phosphorylation [>>9<<,10]. In order to test whether rasKP-induced apoptosis in the eye is mediated by hid, we completely removed hid function by using a null allele in a rasKP mutant and see if it could suppress the small eye phenotype.
n3:mentions: n2:9814704

Subject Item: _:vb6245514
rdf:type: n3:Context
rdf:value: In Drosophila, Ras has been shown to promote cell survival by both down regulating hid expression and inactivating Hid protein through phosphorylation [9,>>10<<]. In order to test whether rasKP-induced apoptosis in the eye is mediated by hid, we completely removed hid function by using a null allele in a rasKP mutant and see if it could suppress the small eye phenotype.
n3:mentions: n2:9814703

Subject Item: _:vb6245515
rdf:type: n3:Context
rdf:value: Consistent with this result, the expression of the baculovirus caspase inhibitor p35, which has been shown to completely block hid-induced apoptosis [>>11<<,29], also only partially suppresses the small eye phenotype of rasKP mutant flies (Figure 4B).
n3:mentions: n2:7622034

Subject Item: _:vb6245516
rdf:type: n3:Context
rdf:value: Consistent with this result, the expression of the baculovirus caspase inhibitor p35, which has been shown to completely block hid-induced apoptosis [11,>>29<<], also only partially suppresses the small eye phenotype of rasKP mutant flies (Figure 4B).
n3:mentions: n2:7925015

Subject Item: _:vb6245517
rdf:type: n3:Context
rdf:value: One prominent candidate is PI3K which has been shown to be a critical effector of Ras in providing an universal survival signal in mammals [>>30<<]. PI3K activates Akt which further phosphorylates a number of substrates involved in the regulation of apoptosis [12]. In the fly, there is also evidence to suggest that the activation of the PI3-K/Akt pathway has antiapoptotic activity
n3:mentions: n2:9529605

Subject Item: _:vb6245518
rdf:type: n3:Context
rdf:value: PI3K activates Akt which further phosphorylates a number of substrates involved in the regulation of apoptosis [>>12<<]. In the fly, there is also evidence to suggest that the activation of the PI3-K/Akt pathway has antiapoptotic activity during embryonic development [9]. To address whether PI3K/Akt activation can rescue the rasKP-induced cell death, we
n3:mentions: n2:10579998

Subject Item: _:vb6245519
rdf:type: n3:Context
rdf:value: In the fly, there is also evidence to suggest that the activation of the PI3-K/Akt pathway has antiapoptotic activity during embryonic development [>>9<<]. To address whether PI3K/Akt activation can rescue the rasKP-induced cell death, we expressed p110, which encodes PI3K, or Akt in rasKP mutant flies. As shown in Figure 4D and 4E, GMR-driven expression of PI3K or Akt cannot significantly
n3:mentions: n2:9814704

Subject Item: _:vb6245520
rdf:type: n3:Context
rdf:value: We tested another candidate antiapoptotic pathway, which utilizes a Drosophila Bcl-2-like protein encoded by the Buffy gene [>>31<<]. In mammals, the Bcl-2 protein prevents the release of cytochrome c from mitochondria, and consequently inhibits the formation of the Apaf-1 apoptosome [32]. As with PI3K/Akt, the overexpression of Buffy also cannot suppress the
n3:mentions: n2:12853472

Subject Item: _:vb6245521
rdf:type: n3:Context
rdf:value: In mammals, the Bcl-2 protein prevents the release of cytochrome c from mitochondria, and consequently inhibits the formation of the Apaf-1 apoptosome [>>32<<]. As with PI3K/Akt, the overexpression of Buffy also cannot suppress the apoptotic eye phenotype of rasKP (Figure 4F).
n3:mentions: n2:9027314

Subject Item: _:vb6245522
rdf:type: n3:Context
rdf:value: In Drosophila, the ERK pathway has been shown to serve as a survival signal that antagonizes JNK signaling from inducing apoptosis [>>33<<]. Thus, it follows that, being an upstream activator of ERK, Ras antiapoptotic activity may lie in its ability to inhibit JNK signaling.
n3:mentions: n2:10490662

Subject Item: _:vb6245523
rdf:type: n3:Context
rdf:value: The activation of the JNK pathway can be achieved by the binding of Eiger to Wengen, which encode, respectively, the mammalian homologs of the tumor necrosis factor TNF and its receptor TNFR [>>16<<,17,34,35].
n3:mentions: n2:12065414

Subject Item: _:vb6245524
rdf:type: n3:Context
rdf:value: The activation of the JNK pathway can be achieved by the binding of Eiger to Wengen, which encode, respectively, the mammalian homologs of the tumor necrosis factor TNF and its receptor TNFR [16,>>17<<,34,35]. We find that RNAi downregulation of Eiger or Wengen also partially rescues the apoptotic eye phenotype of the rasKP mutant (Figure 6E, F). As with the regulation of Hid activity by Ras, we ask if JNK activity is also affected.
n3:mentions: n2:12176339

Subject Item: _:vb6245525
rdf:type: n3:Context
rdf:value: The activation of the JNK pathway can be achieved by the binding of Eiger to Wengen, which encode, respectively, the mammalian homologs of the tumor necrosis factor TNF and its receptor TNFR [16,17,>>34<<,35]. We find that RNAi downregulation of Eiger or Wengen also partially rescues the apoptotic eye phenotype of the rasKP mutant (Figure 6E, F). As with the regulation of Hid activity by Ras, we ask if JNK activity is also affected. When
n3:mentions: n2:12084706

Subject Item: _:vb6245526
rdf:type: n3:Context
rdf:value: The activation of the JNK pathway can be achieved by the binding of Eiger to Wengen, which encode, respectively, the mammalian homologs of the tumor necrosis factor TNF and its receptor TNFR [16,17,34,>>35<<]. We find that RNAi downregulation of Eiger or Wengen also partially rescues the apoptotic eye phenotype of the rasKP mutant (Figure 6E, F). As with the regulation of Hid activity by Ras, we ask if JNK activity is also affected. When eye
n3:mentions: n2:12894227

Subject Item: _:vb6245527
rdf:type: n9:Section
dc:title: methods
n9:contains: _:vb6245528 _:vb6245529 _:vb6245530 _:vb6245531 _:vb6245532

Subject Item: _:vb6245528
rdf:type: n3:Context
rdf:value: The following stocks were kindly provided by our colleagues. rasD38N [>>22<<], rasΔC40b, rasΔC17b, and pR5.5ΔRlb1 [24] (Celeste Berg), UAS-buffy [31] (Helena Richardson), Df (3L)H99 and Hid05014 (Kristin White), UAS-Eiger-IR, UAS-Wengen-IR, UAS-DTRAF1-IR, UAS-DTRAF2-IR, UAS-DTAK1-IR, UAS-Hep-IR, and UAS-BskDN[14]
n3:mentions: n2:1934068

Subject Item: _:vb6245529
rdf:type: n3:Context
rdf:value: rasD38N [22], rasΔC40b, rasΔC17b, and pR5.5ΔRlb1 [>>24<<] (Celeste Berg), UAS-buffy [31] (Helena Richardson), Df (3L)H99 and Hid05014 (Kristin White), UAS-Eiger-IR, UAS-Wengen-IR, UAS-DTRAF1-IR, UAS-DTRAF2-IR, UAS-DTAK1-IR, UAS-Hep-IR, and UAS-BskDN[14] (Tatsushi Igaki).
n3:mentions: n2:8978043

Subject Item: _:vb6245530
rdf:type: n3:Context
rdf:value: rasD38N [22], rasΔC40b, rasΔC17b, and pR5.5ΔRlb1 [24] (Celeste Berg), UAS-buffy [>>31<<] (Helena Richardson), Df (3L)H99 and Hid05014 (Kristin White), UAS-Eiger-IR, UAS-Wengen-IR, UAS-DTRAF1-IR, UAS-DTRAF2-IR, UAS-DTAK1-IR, UAS-Hep-IR, and UAS-BskDN[14] (Tatsushi Igaki).
n3:mentions: n2:12853472

Subject Item: _:vb6245531
rdf:type: n3:Context
rdf:value: rasΔC40b, rasΔC17b, and pR5.5ΔRlb1 [24] (Celeste Berg), UAS-buffy [31] (Helena Richardson), Df (3L)H99 and Hid05014 (Kristin White), UAS-Eiger-IR, UAS-Wengen-IR, UAS-DTRAF1-IR, UAS-DTRAF2-IR, UAS-DTAK1-IR, UAS-Hep-IR, and UAS-BskDN[>>14<<] (Tatsushi Igaki). The UAS-ras, ras85DelB, and all the deficiency lines used in this report were from the Bloomington Drosophila Stock Center.
n3:mentions: n2:16753569

Subject Item: _:vb6245532
rdf:type: n3:Context
rdf:value: Eye disc fixation and staining, as well as adult eye histological section, were performed as described [>>37<<]. Acridine orange staining of third instar larval eye discs was performed according to standard procedure [38].
n3:mentions: n2:7707974

Subject Item: _:vb6245533
rdf:type: n9:Section
dc:title: discussion
n9:contains: _:vb6245534 _:vb6245535 _:vb6245536 _:vb6245537

Subject Item: _:vb6245534
rdf:type: n3:Context
rdf:value: Previous work has suggested that the JNK pathway control cell death by regulating hid expression [>>17<<]. This notion implies that the impact of Ras signaling on the JNK pathway might also converge on Hid activity.
n3:mentions: n2:12176339

Subject Item: _:vb6245535
rdf:type: n3:Context
rdf:value: Previous work has shown that the forced activation of JNK signaling in the developing eye disc can cause widespread cell death [>>16<<,17,36]. However, the normal physiological role of JNK signaling during development is still not clear.
n3:mentions: n2:12065414

Subject Item: _:vb6245536
rdf:type: n3:Context
rdf:value: Previous work has shown that the forced activation of JNK signaling in the developing eye disc can cause widespread cell death [16,>>17<<,36]. However, the normal physiological role of JNK signaling during development is still not clear.
n3:mentions: n2:12176339

Subject Item: _:vb6245537
rdf:type: n3:Context
rdf:value: Previous work has shown that the forced activation of JNK signaling in the developing eye disc can cause widespread cell death [16,17,>>36<<]. However, the normal physiological role of JNK signaling during development is still not clear.
n3:mentions: n2:10757786

Subject Item: _:vb6245538
rdf:type: n9:Section
dc:title: background
n9:contains: _:vb6245548 _:vb6245549 _:vb6245550 _:vb6245551 _:vb6245544 _:vb6245545 _:vb6245546 _:vb6245547 _:vb6245540 _:vb6245541 _:vb6245542 _:vb6245543 _:vb6245539 _:vb6245556 _:vb6245557 _:vb6245552 _:vb6245553 _:vb6245554 _:vb6245555

Subject Item: _:vb6245539
rdf:type: n3:Context
rdf:value: It plays a critical role in normal development where it is required for proper morphogenesis and tissue homeostasis, as well as serving a protective mechanism against extracellular pathogenic agents [>>1<<-3]. Apoptosis is also seen in pathological conditions such as when cells are deprived of survival signals. The biochemical pathway involved in apoptosis has been shown to be conserved from lower organisms, such as Drosophila, to mammals.
n3:mentions: n2:1557121 n2:10408443 n2:10964491

Subject Item: _:vb6245540
rdf:type: n3:Context
rdf:value: Drosophila eye development is one of the best models for studying mechanisms of apoptosis [>>4<<]. The compound eye is composed of about 800 units called ommatidia. Each ommatidium has eight photoreceptor cells and six supporting cells, all differentiated from epithelial cells in the larval eye imaginal disc [5].
n3:mentions: n2:15573123

Subject Item: _:vb6245541
rdf:type: n3:Context
rdf:value: Each ommatidium has eight photoreceptor cells and six supporting cells, all differentiated from epithelial cells in the larval eye imaginal disc [>>5<<]. During late pupal development, excess cells that are not recruited for differentiation are removed by apoptosis. Thus, mutations which cause excessive or insufficient apoptosis will disrupt pattern formation during eye development and,
n3:mentions: n2:12547518

Subject Item: _:vb6245542
rdf:type: n3:Context
rdf:value: Notch signalling is required for apoptosis [>>6<<], while the EGFR/Ras pathway is required for cell survival [7].
n3:mentions: n2:2792755

Subject Item: _:vb6245543
rdf:type: n3:Context
rdf:value: Notch signalling is required for apoptosis [6], while the EGFR/Ras pathway is required for cell survival [>>7<<].
n3:mentions: n2:11257224

Subject Item: _:vb6245544
rdf:type: n3:Context
rdf:value: In Drosophila, Ras signalling is thought to inhibit apoptosis by antagonizing the activity of Hid, which promotes apoptosis through the degradation of the Drosophila Inhibitor of Apoptosis Protein 1 (DIAP1) [>>8<<]. As a consequence of Ras signalling, not only is hid expression reduced, but the Hid protein itself is phosphorylated and becomes inactivated [9,10].
n3:mentions: n2:10481910

Subject Item: _:vb6245545
rdf:type: n3:Context
rdf:value: As a consequence of Ras signalling, not only is hid expression reduced, but the Hid protein itself is phosphorylated and becomes inactivated [>>9<<,10]. Interestingly, although ubiquitous expression of a dominant active form of Ras could inhibit a majority of cell death that occurs normally in the fly embryo, cell death is not completely eliminated even in embryos mutant for a hid
n3:mentions: n2:9814704

Subject Item: _:vb6245546
rdf:type: n3:Context
rdf:value: As a consequence of Ras signalling, not only is hid expression reduced, but the Hid protein itself is phosphorylated and becomes inactivated [9,>>10<<]. Interestingly, although ubiquitous expression of a dominant active form of Ras could inhibit a majority of cell death that occurs normally in the fly embryo, cell death is not completely eliminated even in embryos mutant for a hid null
n3:mentions: n2:9814703

Subject Item: _:vb6245547
rdf:type: n3:Context
rdf:value: although ubiquitous expression of a dominant active form of Ras could inhibit a majority of cell death that occurs normally in the fly embryo, cell death is not completely eliminated even in embryos mutant for a hid null allele [>>10<<,11]. This observation suggests the possibility of a Hid-independent pathway regulating apoptosis, which can be suppressed through other means besides Ras.
n3:mentions: n2:9814703

Subject Item: _:vb6245548
rdf:type: n3:Context
rdf:value: although ubiquitous expression of a dominant active form of Ras could inhibit a majority of cell death that occurs normally in the fly embryo, cell death is not completely eliminated even in embryos mutant for a hid null allele [10,>>11<<]. This observation suggests the possibility of a Hid-independent pathway regulating apoptosis, which can be suppressed through other means besides Ras.
n3:mentions: n2:7622034

Subject Item: _:vb6245549
rdf:type: n3:Context
rdf:value: One of the candidate signals is the PI3K/Akt pathway, which has been shown to regulate apoptosis in mammals and to be a major downstream target of activated Ras [>>12<<]. However, so far there is no evidence to support this hypothesis in Drosophila.
n3:mentions: n2:10579998

Subject Item: _:vb6245550
rdf:type: n3:Context
rdf:value: c-Jun N-terminal protein kinase (JNK) signaling is involved in the regulation of morphogenesis, cell proliferation, cell differentiation, cell migration, and apoptosis, including tumor progression and metastasis [>>13<<-15]. In the fly, JNK-induced apoptosis has an important role in the morphogenesis of the wing imaginal disc during development [1].
n3:mentions: n2:16753569 n2:15704176 n2:11057897

Subject Item: _:vb6245551
rdf:type: n3:Context
rdf:value: In the fly, JNK-induced apoptosis has an important role in the morphogenesis of the wing imaginal disc during development [>>1<<]. During eye development, the overexpression of Eiger, the Drosophila homolog of mammalian TNF, triggers JNK signaling causing the loss of eye tissue as a result of excessive apoptosis [16,17]. Cross-talks have been found between the
n3:mentions: n2:10408443

Subject Item: _:vb6245552
rdf:type: n3:Context
rdf:value: During eye development, the overexpression of Eiger, the Drosophila homolog of mammalian TNF, triggers JNK signaling causing the loss of eye tissue as a result of excessive apoptosis [>>16<<,17]. Cross-talks have been found between the Ras/MAPK and JNK pathways in regulating cell survival and apoptosis [18,19]. In cultured mammalian cells, Raf-1 has been shown to promote cell survival by antagonizing ASK1 [20], a JNK
n3:mentions: n2:12065414

Subject Item: _:vb6245553
rdf:type: n3:Context
rdf:value: During eye development, the overexpression of Eiger, the Drosophila homolog of mammalian TNF, triggers JNK signaling causing the loss of eye tissue as a result of excessive apoptosis [16,>>17<<]. Cross-talks have been found between the Ras/MAPK and JNK pathways in regulating cell survival and apoptosis [18,19]. In cultured mammalian cells, Raf-1 has been shown to promote cell survival by antagonizing ASK1 [20], a JNK activator
n3:mentions: n2:12176339

Subject Item: _:vb6245554
rdf:type: n3:Context
rdf:value: Cross-talks have been found between the Ras/MAPK and JNK pathways in regulating cell survival and apoptosis [>>18<<,19]. In cultured mammalian cells, Raf-1 has been shown to promote cell survival by antagonizing ASK1 [20], a JNK activator [21].
n3:mentions: n2:10048301

Subject Item: _:vb6245555
rdf:type: n3:Context
rdf:value: Cross-talks have been found between the Ras/MAPK and JNK pathways in regulating cell survival and apoptosis [18,>>19<<]. In cultured mammalian cells, Raf-1 has been shown to promote cell survival by antagonizing ASK1 [20], a JNK activator [21].
n3:mentions: n2:7481820

Subject Item: _:vb6245556
rdf:type: n3:Context
rdf:value: In cultured mammalian cells, Raf-1 has been shown to promote cell survival by antagonizing ASK1 [>>20<<], a JNK activator [21].
n3:mentions: n2:11427728

Subject Item: _:vb6245557
rdf:type: n3:Context
rdf:value: In cultured mammalian cells, Raf-1 has been shown to promote cell survival by antagonizing ASK1 [20], a JNK activator [>>21<<].
n3:mentions: n2:11607847

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