Reference Report

Reference
Citation	Peretz, G., Bakhrat, A., Abdu, U. (2007). Expression of the Drosophila melanogaster GADD45 homolog (CG11086) affects egg asymmetric development that is mediated by the c-Jun N-terminal kinase pathway. Genetics 177(3): 1691--1702. (Export to RIS)
FlyBase ID	FBrf0201501
Publication Type	Research paper
PubMed ID	18039880
PubMed Abstract	The mammalian GADD45 (growth arrest and DNA-damage inducible) gene family is composed of three highly homologous small, acidic, nuclear proteins: GADD45alpha, GADD45beta, and GADD45gamma. GADD45 proteins are involved in important processes such as regulation of DNA repair, cell cycle control, and apoptosis. Annotation of the Drosophila melanogaster genome revealed that it contains a single GADD45-like protein (CG11086; D-GADD45). We found that, as its mammalian homologs, D-GADD45 is a nuclear protein; however, D-GADD45 expression is not elevated following exposure to genotoxic and nongenotoxic agents in Schneider cells and in adult flies. We showed that the D-GADD45 transcript increased following immune response activation, consistent with previous microarray findings. Since upregulation of GADD45 proteins has been characterized as an important cellular response to genotoxic and nongenotoxic agents, we aimed to characterize the effect of D-GADD45 overexpression on D. melanogaster development. Overexpression of D-GADD45 in various tissues led to different phenotypic responses. Specifically, in the somatic follicle cells overexpression caused apoptosis, while overexpression in the germline affected the dorsal-ventral polarity of the eggshell and disrupted the localization of anterior-posterior polarity determinants. In this article we focused on the role of D-GADD45 overexpression in the germline and found that D-GADD45 caused dorsalization of the eggshell. Since mammalian GADD45 proteins are activators of the c-Jun N-terminal kinase (JNK)/p38 mitogen-activated protein kinase (MAPK) signaling pathways, we tested for a genetic interaction in D. melanogaster. We found that eggshell polarity defects caused by D-GADD45 overexpression were dominantly suppressed by mutations in the JNK pathway, suggesting that the JNK pathway has a novel, D-GADD45-mediated, function in the Drosophila germline.
DOI	10.1534/genetics.107.079517
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Language of Publication	English
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Publication Type	Journal
Abbreviation	Genetics
Title	Genetics
Publication Year	1916-
ISBN/ISSN	0016-6731
Data from Reference
Aberrations (1)
	Df(1)H6
Alleles (16)
	Ecol\lacZ^kek1-BB142 Ecol\lacZ^KZ503 Gadd45^{Scer\UAS.P\T.cPa} hep^G0208 hep^H6 hep^r75 Khc::nod^143.2 lic^H6 Scer\GAL4^32B Scer\GAL4^Act5C.PU Scer\GAL4^CY2 Scer\GAL4^GMR.PF Scer\GAL4^GR1 Scer\GAL4^{nos.UTR.T:Hsim\VP16} Scer\GAL4^tub.PU w^+mC
Constructs (5)
	P{Act5C-GAL4.U} P{GAL4::VP16-nos.UTR} P{GAL4-ninaE.GMR} P{tub-GAL4.U} P{UASp-Gadd45.P}
Genes (14)
	bcd br Drs Ecol\lacZ Gadd45 grk hep kek1 Khc::nod Lam lic osk Scer\GAL4 w
Insertions (6)
	P{GawB}32B P{GawB}CY2 P{GawB}GR1 P{KZ.TRAP}KZ503 P{lacW}BB142 P{NZ}143.2
Natural transposons (1)
	P-element