Extramacrochaetae regulates Notch signaling in the Drosophila eye through non-apoptotic caspase activity
Many cell fate decisions are determined transcriptionally. Accordingly, some fate specification is prevented by Inhibitor of DNA-binding (Id) proteins that interfere with DNA binding by master regulatory transcription factors. We show that the Drosophila Id protein Extra macrochaetae (Emc) also affe...
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eLife Sciences Publications Ltd
2024-11-01
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| Online Access: | https://elifesciences.org/articles/91988 |
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| author | Sudershana Nair Nicholas E Baker |
| author_facet | Sudershana Nair Nicholas E Baker |
| author_sort | Sudershana Nair |
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| description | Many cell fate decisions are determined transcriptionally. Accordingly, some fate specification is prevented by Inhibitor of DNA-binding (Id) proteins that interfere with DNA binding by master regulatory transcription factors. We show that the Drosophila Id protein Extra macrochaetae (Emc) also affects developmental decisions by regulating caspase activity. Emc, which prevents proneural bHLH transcription factors from specifying neural cell fate, also prevents homodimerization of another bHLH protein, Daughterless (Da), and thereby maintains expression of the Death-Associated Inhibitor of Apoptosis (diap1) gene. Accordingly, we found that multiple effects of emc mutations on cell growth and on eye development were all caused by activation of caspases. These effects included acceleration of the morphogenetic furrow, failure of R7 photoreceptor cell specification, and delayed differentiation of non-neuronal cone cells. Within emc mutant clones, Notch signaling was elevated in the morphogenetic furrow, increasing morphogenetic furrow speed. This was associated with caspase-dependent increase in levels of Delta protein, the transmembrane ligand for Notch. Posterior to the morphogenetic furrow, elevated Delta cis-inhibited Notch signaling that was required for R7 specification and cone cell differentiation. Growth inhibition of emc mutant clones in wing imaginal discs also depended on caspases. Thus, emc mutations reveal the importance of restraining caspase activity even in non-apoptotic cells to prevent abnormal development, in the Drosophila eye through effects on Notch signaling. |
| format | Article |
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| institution | Kabale University |
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| language | English |
| publishDate | 2024-11-01 |
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| spelling | doaj-art-9ac920143de8498a85c89794e8b487062025-02-03T14:11:30ZengeLife Sciences Publications LtdeLife2050-084X2024-11-011210.7554/eLife.91988Extramacrochaetae regulates Notch signaling in the Drosophila eye through non-apoptotic caspase activitySudershana Nair0Nicholas E Baker1https://orcid.org/0000-0002-4250-3488Department of Genetics, Albert Einstein College of Medicine, Bronx, United StatesDepartment of Genetics, Albert Einstein College of Medicine, Bronx, United States; Department of Developmental and Molecular Biology, Albert Einstein College of Medicine, Bronx, United States; Department of Ophthalmology and Visual Sciences, Albert Einstein College of Medicine, Bronx, United StatesMany cell fate decisions are determined transcriptionally. Accordingly, some fate specification is prevented by Inhibitor of DNA-binding (Id) proteins that interfere with DNA binding by master regulatory transcription factors. We show that the Drosophila Id protein Extra macrochaetae (Emc) also affects developmental decisions by regulating caspase activity. Emc, which prevents proneural bHLH transcription factors from specifying neural cell fate, also prevents homodimerization of another bHLH protein, Daughterless (Da), and thereby maintains expression of the Death-Associated Inhibitor of Apoptosis (diap1) gene. Accordingly, we found that multiple effects of emc mutations on cell growth and on eye development were all caused by activation of caspases. These effects included acceleration of the morphogenetic furrow, failure of R7 photoreceptor cell specification, and delayed differentiation of non-neuronal cone cells. Within emc mutant clones, Notch signaling was elevated in the morphogenetic furrow, increasing morphogenetic furrow speed. This was associated with caspase-dependent increase in levels of Delta protein, the transmembrane ligand for Notch. Posterior to the morphogenetic furrow, elevated Delta cis-inhibited Notch signaling that was required for R7 specification and cone cell differentiation. Growth inhibition of emc mutant clones in wing imaginal discs also depended on caspases. Thus, emc mutations reveal the importance of restraining caspase activity even in non-apoptotic cells to prevent abnormal development, in the Drosophila eye through effects on Notch signaling.https://elifesciences.org/articles/91988extramacrochaetaeID proteincaspasenon-apoptotic caspaseDeltaDrosophila eye |
| spellingShingle | Sudershana Nair Nicholas E Baker Extramacrochaetae regulates Notch signaling in the Drosophila eye through non-apoptotic caspase activity eLife extramacrochaetae ID protein caspase non-apoptotic caspase Delta Drosophila eye |
| title | Extramacrochaetae regulates Notch signaling in the Drosophila eye through non-apoptotic caspase activity |
| title_full | Extramacrochaetae regulates Notch signaling in the Drosophila eye through non-apoptotic caspase activity |
| title_fullStr | Extramacrochaetae regulates Notch signaling in the Drosophila eye through non-apoptotic caspase activity |
| title_full_unstemmed | Extramacrochaetae regulates Notch signaling in the Drosophila eye through non-apoptotic caspase activity |
| title_short | Extramacrochaetae regulates Notch signaling in the Drosophila eye through non-apoptotic caspase activity |
| title_sort | extramacrochaetae regulates notch signaling in the drosophila eye through non apoptotic caspase activity |
| topic | extramacrochaetae ID protein caspase non-apoptotic caspase Delta Drosophila eye |
| url | https://elifesciences.org/articles/91988 |
| work_keys_str_mv | AT sudershananair extramacrochaetaeregulatesnotchsignalinginthedrosophilaeyethroughnonapoptoticcaspaseactivity AT nicholasebaker extramacrochaetaeregulatesnotchsignalinginthedrosophilaeyethroughnonapoptoticcaspaseactivity |