GLYAT regulates JNK-mediated cell death in Drosophila

Abstract Cell death is a fundamental progress that regulates cell number, tissue homeostasis and organ size in development. The c-Jun N-terminal kinase (JNK) pathway has been evolutionarily conserved from fly to human, and plays essential roles in regulating cell death. To characterize additional ge...

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Autores principales:	Pu Ren, Wenzhe Li, Lei Xue
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2017
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/074d283570654146a2b20637a842f51d
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spelling	oai:doaj.org-article:074d283570654146a2b20637a842f51d2021-12-02T16:06:59ZGLYAT regulates JNK-mediated cell death in Drosophila10.1038/s41598-017-05482-y2045-2322https://doaj.org/article/074d283570654146a2b20637a842f51d2017-07-01T00:00:00Zhttps://doi.org/10.1038/s41598-017-05482-yhttps://doaj.org/toc/2045-2322Abstract Cell death is a fundamental progress that regulates cell number, tissue homeostasis and organ size in development. The c-Jun N-terminal kinase (JNK) pathway has been evolutionarily conserved from fly to human, and plays essential roles in regulating cell death. To characterize additional genes that regulate JNK signaling, we performed a genetic screen in Drosophila and identified dGLYAT, a novel gene whose function was previously unknown, as a modulator of JNK-mediated cell death. We found that loss of dGLYAT suppressed JNK activation and cell death triggered by over-expression of Egr or Hep, or depletion of puc or lgl in development, suggesting dGLYAT regulates both ectopic and physiological functions of JNK pathway. Furthermore, we showed that loss of dGLYAT inhibits JNK-mediated ROS production, suggesting dGLYAT regulates multiple functions of JNK signaling in vivo.Pu RenWenzhe LiLei XueNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 7, Iss 1, Pp 1-9 (2017)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Pu Ren Wenzhe Li Lei Xue GLYAT regulates JNK-mediated cell death in Drosophila
description	Abstract Cell death is a fundamental progress that regulates cell number, tissue homeostasis and organ size in development. The c-Jun N-terminal kinase (JNK) pathway has been evolutionarily conserved from fly to human, and plays essential roles in regulating cell death. To characterize additional genes that regulate JNK signaling, we performed a genetic screen in Drosophila and identified dGLYAT, a novel gene whose function was previously unknown, as a modulator of JNK-mediated cell death. We found that loss of dGLYAT suppressed JNK activation and cell death triggered by over-expression of Egr or Hep, or depletion of puc or lgl in development, suggesting dGLYAT regulates both ectopic and physiological functions of JNK pathway. Furthermore, we showed that loss of dGLYAT inhibits JNK-mediated ROS production, suggesting dGLYAT regulates multiple functions of JNK signaling in vivo.
format	article
author	Pu Ren Wenzhe Li Lei Xue
author_facet	Pu Ren Wenzhe Li Lei Xue
author_sort	Pu Ren
title	GLYAT regulates JNK-mediated cell death in Drosophila
title_short	GLYAT regulates JNK-mediated cell death in Drosophila
title_full	GLYAT regulates JNK-mediated cell death in Drosophila
title_fullStr	GLYAT regulates JNK-mediated cell death in Drosophila
title_full_unstemmed	GLYAT regulates JNK-mediated cell death in Drosophila
title_sort	glyat regulates jnk-mediated cell death in drosophila
publisher	Nature Portfolio
publishDate	2017
url	https://doaj.org/article/074d283570654146a2b20637a842f51d
work_keys_str_mv	AT puren glyatregulatesjnkmediatedcelldeathindrosophila AT wenzheli glyatregulatesjnkmediatedcelldeathindrosophila AT leixue glyatregulatesjnkmediatedcelldeathindrosophila
_version_	1718384758927392768

GLYAT regulates JNK-mediated cell death in Drosophila

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