Reference Report

Reference
Citation	Centanin, L., Ratcliffe, P.J., Wappner, P. (2005). Reversion of lethality and growth defects in Fatiga oxygen-sensor mutant flies by loss of Hypoxia-Inducible Factor-alpha/Sima. EMBO Rep. 6(11): 1070--1075. (Export to RIS)
FlyBase ID	FBrf0190371
Publication Type	Research paper
PubMed ID	16179946
PubMed Abstract	Hypoxia-Inducible Factor (HIF) prolyl hydroxylase domains (PHDs) have been proposed to act as sensors that have an important role in oxygen homeostasis. In the presence of oxygen, they hydroxylate two specific prolyl residues in HIF-alpha polypeptides, thereby promoting their proteasomal degradation. So far, however, the developmental consequences of the inactivation of PHDs in higher metazoans have not been reported. Here, we describe novel loss-of-function mutants of fatiga, the gene encoding the Drosophila PHD oxygen sensor, which manifest growth defects and lethality. We also report a null mutation in dHIF-alpha/sima, which is unable to adapt to hypoxia but is fully viable in normoxic conditions. Strikingly, loss-of-function mutations of sima rescued the developmental defects observed in fatiga mutants and enabled survival to adulthood. These results indicate that the main functions of Fatiga in development, including control of cell size, involve the regulation of dHIF/Sima.
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Language of Publication	English
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Publication Type	Journal
Abbreviation	EMBO Rep.
Title	EMBO Reports
Publication Year	2000-
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Data from Reference
Alleles (14)
	Ecol\lacZ^{Mmus\Ldh1.233} Hph¹ Hph⁹ Hph⁶⁴ Hph⁰²²⁵⁵ Scer\GAL4^Act5C.PP Scer\GAL4^bs-23.26 Scer\GAL4^btl.PS Scer\GAL4^esg-p127 Scer\GAL4^hs.PB Scer\GAL4^Mmus\Ldh1.51 Scer\GAL4^{Scer\FRT.Rnor\CD2.Act5C} sima^KG07607 sima^Scer\UAS.cBa
Constructs (8)
	P{?PZ} P{GAL4-Act5C(FRT.CD2).P} P{GAL4-bs.23.26} P{GAL4-btl.S} P{GAL4-Hsp70.PB} P{LDH-Gal4.51} P{LDH-lacZ.233} P{UAS-sima.B}
Genes (4)
	Ecol\lacZ Hph Scer\GAL4 sima
Insertions (5)
	P{?PZ}Hph¹ P{?PZ}Hph⁹ P{GawB}p127 P{PZ}Hph⁰²²⁵⁵ P{SUPor-P}sima^KG07607