author_facet Duan, Hong
de Navas, Luis F.
Hu, Fuqu
Sun, Kailiang
Mavromatakis, Yannis E.
Viets, Kayla
Zhou, Cyrus
Kavaler, Joshua
Johnston, Robert J.
Tomlinson, Andrew
Lai, Eric C.
Duan, Hong
de Navas, Luis F.
Hu, Fuqu
Sun, Kailiang
Mavromatakis, Yannis E.
Viets, Kayla
Zhou, Cyrus
Kavaler, Joshua
Johnston, Robert J.
Tomlinson, Andrew
Lai, Eric C.
author Duan, Hong
de Navas, Luis F.
Hu, Fuqu
Sun, Kailiang
Mavromatakis, Yannis E.
Viets, Kayla
Zhou, Cyrus
Kavaler, Joshua
Johnston, Robert J.
Tomlinson, Andrew
Lai, Eric C.
spellingShingle Duan, Hong
de Navas, Luis F.
Hu, Fuqu
Sun, Kailiang
Mavromatakis, Yannis E.
Viets, Kayla
Zhou, Cyrus
Kavaler, Joshua
Johnston, Robert J.
Tomlinson, Andrew
Lai, Eric C.
Development
The mir-279/996 cluster represses receptor tyrosine kinase signaling to determine cell fates in the Drosophila eye
Developmental Biology
Molecular Biology
author_sort duan, hong
spelling Duan, Hong de Navas, Luis F. Hu, Fuqu Sun, Kailiang Mavromatakis, Yannis E. Viets, Kayla Zhou, Cyrus Kavaler, Joshua Johnston, Robert J. Tomlinson, Andrew Lai, Eric C. 1477-9129 0950-1991 The Company of Biologists Developmental Biology Molecular Biology http://dx.doi.org/10.1242/dev.159053 <jats:p>Photoreceptors in the crystalline Drosophila eye are recruited by receptor tyrosine kinase (RTK)/Ras signaling, mediated by the Epidermal Growth Factor receptor (EGFR) and Sevenless receptor. Analyses of an allelic deletion series of the mir-279/996 locus, along with a panel of modified genomic rescue transgenes, show that normal Drosophila eye patterning depends on both miRNAs. Transcriptional reporter and activity sensor transgenes reveal expression and function of miR-279/996 in non-neural cells of the developing eye. Moreover, mir-279/996 mutants exhibit substantial numbers of ectopic photoreceptors, particularly of R7, and cone cell loss. These miRNAs restrict RTK signaling in the eye, since mir-279/996 nulls are dominantly suppressed by positive components of the EGFR pathway and enhanced by heterozygosity for an EGFR repressor. miR-279/996 limit photoreceptor recruitment by targeting multiple positive RTK/Ras signaling components that promote photoreceptor/R7 specification. Strikingly, deletion of mir-279/996 sufficiently de-represses RTK/Ras signaling so as to rescue a population of R7 cells in R7-specific RTK null mutants boss and sev, which otherwise completely lack this cell fate. Altogether, we reveal a rare setting of developmental cell specification that substantially requires miRNA control.</jats:p> The <i>mir-279/996</i> cluster represses receptor tyrosine kinase signaling to determine cell fates in the <i>Drosophila</i> eye Development
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title The mir-279/996 cluster represses receptor tyrosine kinase signaling to determine cell fates in the Drosophila eye
title_unstemmed The mir-279/996 cluster represses receptor tyrosine kinase signaling to determine cell fates in the Drosophila eye
title_full The mir-279/996 cluster represses receptor tyrosine kinase signaling to determine cell fates in the Drosophila eye
title_fullStr The mir-279/996 cluster represses receptor tyrosine kinase signaling to determine cell fates in the Drosophila eye
title_full_unstemmed The mir-279/996 cluster represses receptor tyrosine kinase signaling to determine cell fates in the Drosophila eye
title_short The mir-279/996 cluster represses receptor tyrosine kinase signaling to determine cell fates in the Drosophila eye
title_sort the <i>mir-279/996</i> cluster represses receptor tyrosine kinase signaling to determine cell fates in the <i>drosophila</i> eye
topic Developmental Biology
Molecular Biology
url http://dx.doi.org/10.1242/dev.159053
publishDate 2018
physical
description <jats:p>Photoreceptors in the crystalline Drosophila eye are recruited by receptor tyrosine kinase (RTK)/Ras signaling, mediated by the Epidermal Growth Factor receptor (EGFR) and Sevenless receptor. Analyses of an allelic deletion series of the mir-279/996 locus, along with a panel of modified genomic rescue transgenes, show that normal Drosophila eye patterning depends on both miRNAs. Transcriptional reporter and activity sensor transgenes reveal expression and function of miR-279/996 in non-neural cells of the developing eye. Moreover, mir-279/996 mutants exhibit substantial numbers of ectopic photoreceptors, particularly of R7, and cone cell loss. These miRNAs restrict RTK signaling in the eye, since mir-279/996 nulls are dominantly suppressed by positive components of the EGFR pathway and enhanced by heterozygosity for an EGFR repressor. miR-279/996 limit photoreceptor recruitment by targeting multiple positive RTK/Ras signaling components that promote photoreceptor/R7 specification. Strikingly, deletion of mir-279/996 sufficiently de-represses RTK/Ras signaling so as to rescue a population of R7 cells in R7-specific RTK null mutants boss and sev, which otherwise completely lack this cell fate. Altogether, we reveal a rare setting of developmental cell specification that substantially requires miRNA control.</jats:p>
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author Duan, Hong, de Navas, Luis F., Hu, Fuqu, Sun, Kailiang, Mavromatakis, Yannis E., Viets, Kayla, Zhou, Cyrus, Kavaler, Joshua, Johnston, Robert J., Tomlinson, Andrew, Lai, Eric C.
author_facet Duan, Hong, de Navas, Luis F., Hu, Fuqu, Sun, Kailiang, Mavromatakis, Yannis E., Viets, Kayla, Zhou, Cyrus, Kavaler, Joshua, Johnston, Robert J., Tomlinson, Andrew, Lai, Eric C., Duan, Hong, de Navas, Luis F., Hu, Fuqu, Sun, Kailiang, Mavromatakis, Yannis E., Viets, Kayla, Zhou, Cyrus, Kavaler, Joshua, Johnston, Robert J., Tomlinson, Andrew, Lai, Eric C.
author_sort duan, hong
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description <jats:p>Photoreceptors in the crystalline Drosophila eye are recruited by receptor tyrosine kinase (RTK)/Ras signaling, mediated by the Epidermal Growth Factor receptor (EGFR) and Sevenless receptor. Analyses of an allelic deletion series of the mir-279/996 locus, along with a panel of modified genomic rescue transgenes, show that normal Drosophila eye patterning depends on both miRNAs. Transcriptional reporter and activity sensor transgenes reveal expression and function of miR-279/996 in non-neural cells of the developing eye. Moreover, mir-279/996 mutants exhibit substantial numbers of ectopic photoreceptors, particularly of R7, and cone cell loss. These miRNAs restrict RTK signaling in the eye, since mir-279/996 nulls are dominantly suppressed by positive components of the EGFR pathway and enhanced by heterozygosity for an EGFR repressor. miR-279/996 limit photoreceptor recruitment by targeting multiple positive RTK/Ras signaling components that promote photoreceptor/R7 specification. Strikingly, deletion of mir-279/996 sufficiently de-represses RTK/Ras signaling so as to rescue a population of R7 cells in R7-specific RTK null mutants boss and sev, which otherwise completely lack this cell fate. Altogether, we reveal a rare setting of developmental cell specification that substantially requires miRNA control.</jats:p>
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spelling Duan, Hong de Navas, Luis F. Hu, Fuqu Sun, Kailiang Mavromatakis, Yannis E. Viets, Kayla Zhou, Cyrus Kavaler, Joshua Johnston, Robert J. Tomlinson, Andrew Lai, Eric C. 1477-9129 0950-1991 The Company of Biologists Developmental Biology Molecular Biology http://dx.doi.org/10.1242/dev.159053 <jats:p>Photoreceptors in the crystalline Drosophila eye are recruited by receptor tyrosine kinase (RTK)/Ras signaling, mediated by the Epidermal Growth Factor receptor (EGFR) and Sevenless receptor. Analyses of an allelic deletion series of the mir-279/996 locus, along with a panel of modified genomic rescue transgenes, show that normal Drosophila eye patterning depends on both miRNAs. Transcriptional reporter and activity sensor transgenes reveal expression and function of miR-279/996 in non-neural cells of the developing eye. Moreover, mir-279/996 mutants exhibit substantial numbers of ectopic photoreceptors, particularly of R7, and cone cell loss. These miRNAs restrict RTK signaling in the eye, since mir-279/996 nulls are dominantly suppressed by positive components of the EGFR pathway and enhanced by heterozygosity for an EGFR repressor. miR-279/996 limit photoreceptor recruitment by targeting multiple positive RTK/Ras signaling components that promote photoreceptor/R7 specification. Strikingly, deletion of mir-279/996 sufficiently de-represses RTK/Ras signaling so as to rescue a population of R7 cells in R7-specific RTK null mutants boss and sev, which otherwise completely lack this cell fate. Altogether, we reveal a rare setting of developmental cell specification that substantially requires miRNA control.</jats:p> The <i>mir-279/996</i> cluster represses receptor tyrosine kinase signaling to determine cell fates in the <i>Drosophila</i> eye Development
spellingShingle Duan, Hong, de Navas, Luis F., Hu, Fuqu, Sun, Kailiang, Mavromatakis, Yannis E., Viets, Kayla, Zhou, Cyrus, Kavaler, Joshua, Johnston, Robert J., Tomlinson, Andrew, Lai, Eric C., Development, The mir-279/996 cluster represses receptor tyrosine kinase signaling to determine cell fates in the Drosophila eye, Developmental Biology, Molecular Biology
title The mir-279/996 cluster represses receptor tyrosine kinase signaling to determine cell fates in the Drosophila eye
title_full The mir-279/996 cluster represses receptor tyrosine kinase signaling to determine cell fates in the Drosophila eye
title_fullStr The mir-279/996 cluster represses receptor tyrosine kinase signaling to determine cell fates in the Drosophila eye
title_full_unstemmed The mir-279/996 cluster represses receptor tyrosine kinase signaling to determine cell fates in the Drosophila eye
title_short The mir-279/996 cluster represses receptor tyrosine kinase signaling to determine cell fates in the Drosophila eye
title_sort the <i>mir-279/996</i> cluster represses receptor tyrosine kinase signaling to determine cell fates in the <i>drosophila</i> eye
title_unstemmed The mir-279/996 cluster represses receptor tyrosine kinase signaling to determine cell fates in the Drosophila eye
topic Developmental Biology, Molecular Biology
url http://dx.doi.org/10.1242/dev.159053