fusilli, an essential gene with a maternal role in Drosophila embryonic dorsal-ventral patterning Journal Article

  

Authors:	Wakabayashi-Ito, N.; Belvin, M. P.; Bluestein, D. A.; Anderson, K. V.
Article Title:	fusilli, an essential gene with a maternal role in Drosophila embryonic dorsal-ventral patterning
Abstract:	The Drosophila fusilli (fus) gene was identified in a genetic screen for dominant maternal enhancers of an unusual dorsalizing mutation in the cactus gene, cact(E10). While females that are heterozygous for the cact(E10) allele produce embryos with wild-type dorsal-ventral patterning, more than 90% of the embryos produced by females that are heterozygous for both cact(E10) and the fus(1) mutation are weakly dorsalized, Loss of fusilli activity causes lethality during embryogenesis but not dorsal-ventral patterning defects, indicating that fusilli is important in more than one developmental process. The fusilli gene encodes a protein with RNA binding motifs related to those in mammalian hnRNP F and H, which play roles in regulated RNA splicing. The fusilli RNA is not present in the oocyte or early embryo, and germ-line clones of fusilli mutations have no maternal effect on dorsal-ventral patterning, indicating that the fusilli maternal effect does not depend on germ-line expression of the gene. Because the fusilli RNA is present in ovarian follicle cells, we propose that fusilli acts downstream of the Drosophila EGF receptor to control the biogenesis of follicle cell transcripts that control the initial dorsal-ventral asymmetry of the embryo. (C) 2001 Academic Press.
Keywords:	embryo; protein; drosophila; receptor; polarity; egf; messenger-rna; nuclear-localization; signaling pathway; melanogaster; dorsal-ventral pattern; follicle cells; hnrnp; cactus; dorsoventral pattern; 2nd chromosome; hnrnp-f; degradation establishes
Journal Title:	Developmental Biology
Volume:	229
Issue:	1
ISSN:	0012-1606
Publisher:	Elsevier Inc.
Date Published:	2001-01-01
Start Page:	44
End Page:	54
Language:	English
ACCESSION:	WOS:000166329500004
DOI:	10.1006/dbio.2000.9954
PROVIDER:	wos
PUBMED:	11133153
Notes:	Article -- Source: Wos

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