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1.
Cell Tissue Res ; 336(1): 149-58, 2009 Apr.
Artículo en Inglés | MEDLINE | ID: mdl-19252929

RESUMEN

In a genetic screen, alpha-4GT1 has been identified as a potential enhancer of Hairless-mediated cell death in the eye of Drosophila. alpha-4GT1 encodes an alpha-1,4-glycosyltransferase, known to catalyze the fifth step in a series of ceramide glycosylation events. As reported for other enzymes involved in the glycosylation of ceramide, alpha-4GT1 is strongly expressed during oogenesis and is deposited maternally in the egg. Moreover, the protein is enriched at cell membranes. Unexpectedly, overexpression of alpha-4GT1 does not enhance Hairless-mediated cell death; instead, Hairless enhancement is caused by an allele of Scutoid present on the alpha-4GT1 chromosome. Interestingly, the downregulation of alpha-4GT1 during eye development amplifies cell death induction by the pro-apoptotic gene reaper. Accordingly, overexpression of alpha-4GT1 represses reaper-induced cell death. Thus, alpha-4GT1 appears to be an inhibitor of apoptosis, as has previously been observed for other ceramide glycosylating enzymes, suggesting that it likewise contributes to ceramide anchoring in the membrane.


Asunto(s)
Apoptosis/genética , Proteínas de Drosophila/fisiología , Drosophila/enzimología , Ojo/embriología , Glicosiltransferasas/fisiología , Fenómenos Fisiológicos Oculares/genética , Animales , Animales Modificados Genéticamente , Apoptosis/efectos de los fármacos , Cruzamientos Genéticos , Regulación hacia Abajo/efectos de los fármacos , Regulación hacia Abajo/genética , Drosophila/embriología , Drosophila/genética , Drosophila/metabolismo , Proteínas de Drosophila/antagonistas & inhibidores , Proteínas de Drosophila/genética , Proteínas de Drosophila/metabolismo , Embrión no Mamífero , Epistasis Genética/fisiología , Ojo/efectos de los fármacos , Ojo/metabolismo , Expresión Génica , Glicosiltransferasas/genética , Glicosiltransferasas/metabolismo , Modelos Biológicos , Fenómenos Fisiológicos Oculares/efectos de los fármacos , ARN Interferente Pequeño/farmacología
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