Reference Report

Reference
Citation	Shibata, T., Ariki, S., Shinzawa, N., Miyaji, R., Suyama, H., Sako, M., Inomata, N., Koshiba, T., Kanuka, H., Kawabata, S. (2010). Protein crosslinking by transglutaminase controls cuticle morphogenesis in Drosophila. PLoS ONE 5(10): e13477. (Export to RIS)
FlyBase ID	FBrf0212149
Publication Type	Research paper
PubMed ID	20976106
PubMed Abstract	Transglutaminase (TG) plays important and diverse roles in mammals, such as blood coagulation and formation of the skin barrier, by catalyzing protein crosslinking. In invertebrates, TG is known to be involved in immobilization of invading pathogens at sites of injury. Here we demonstrate that Drosophila TG is an important enzyme for cuticle morphogenesis. Although TG activity was undetectable before the second instar larval stage, it dramatically increased in the third instar larval stage. RNA interference (RNAi) of the TG gene caused a pupal semi-lethal phenotype and abnormal morphology. Furthermore, TG-RNAi flies showed a significantly shorter life span than their counterparts, and approximately 90% of flies died within 30 days after eclosion. Stage-specific TG-RNAi before the third instar larval stage resulted in cuticle abnormality, but the TG-RNAi after the late pupal stage did not, indicating that TG plays a key role at or before the early pupal stage. Immediately following eclosion, acid-extractable protein from wild-type wings was nearly all converted to non-extractable protein due to wing maturation, whereas several proteins remained acid-extractable in the mature wings of TG-RNAi flies. We identified four proteins--two cuticular chitin-binding proteins, larval serum protein 2, and a putative C-type lectin-as TG substrates. RNAi of their corresponding genes caused a lethal phenotype or cuticle abnormality. Our results indicate that TG-dependent protein crosslinking in Drosophila plays a key role in cuticle morphogenesis and sclerotization.
DOI	10.1371/journal.pone.0013477
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Language of Publication	English
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Publication Type	Journal
Abbreviation	PLoS ONE
Title	PLoS ONE
Publication Year	2006-
ISBN/ISSN	1932-6203
Data from Reference
Alleles (9)
	Clect27^NIG.3244R Cpr76Bd^NIG.9299R Cpr97Eb^GD5674 Lsp2^NIG.6806R Scer\GAL4^Bx-MS1096 Scer\GAL4^da.G32 Scer\GAL80^ts.αTub84B Tg^NIG.7356R Tg^Scer\UAS.cIa
Constructs (8)
	P{GAL4-da.G32} P{GD5674} P{NIG.3244R} P{NIG.6806R} P{NIG.7356R} P{NIG.9299R} P{tubP-GAL80^ts} P{UAS-Tg.I}
Genes (15)
	Clect27 Cpr47Ef Cpr64Ac Cpr76Bd Cpr97Eb Fer1HCH Fer2LCH Gasp Idgf4 Lsp2 Rfabg Scer\GAL4 Scer\GAL80 Tg Tsf1
Insertions (1)
	P{GawB}Bx^MS1096
Natural transposons (1)
	P-element