Abstract:
:As the germ band shortens in Drosophila melanogaster embryos, cell shape changes cause segments to narrow anteroposteriorly and to lengthen dorsoventrally. One of the genes required for this retraction process is the hindsight (hnt) gene. hnt encodes a nuclear Zinc-finger protein that is expressed in the extraembryonic amnioserosa and the endodermal midgut prior to and during germ band retraction (M. L. R. Yip, M. L. Lamka, and H. D. Lipshitz, 1997, Development 124, 2129-2141). Here we show, through analysis of hnt genetic mosaic embryos, that hnt activity in the amnioserosa-particularly in those cells that are adjacent to the epidermis-is necessary for germ band retraction. In hnt mutant embryos the amnioserosa undergoes premature cell death (L. C. Frank and C. Rushlow, 1996, Development 122, 1343-1352). We demonstrate that prevention of premature apoptosis in hnt mutants does not rescue retraction. Thus, failure of this process is not an indirect consequence of premature amnioserosal apoptosis; instead, hnt must function in a pathway that controls germ band retraction. We show that the Krüppel gene is activated by hnt in the amnioserosa while the Drosophila insulin receptor (INR) functions downstream of hnt in the germ band. We present evidence against a physical model in which the amnioserosa "pushes" the germ band during retraction. Rather, it is likely that the amnioserosa functions in production, activation, or presentation of a diffusible signal required for retraction.
journal_name
Dev Bioljournal_title
Developmental biologyauthors
Lamka ML,Lipshitz HDdoi
10.1006/dbio.1999.9409subject
Has Abstractpub_date
1999-10-01 00:00:00pages
102-12issue
1eissn
0012-1606issn
1095-564Xpii
S0012-1606(99)99409-5journal_volume
214pub_type
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