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Published June 1993 | Published
Journal Article Open

Dynamic Hsp83 RNA localization during Drosophila oogenesis and embryogenesis


Hsp83 is the Drosophila homolog of the mammalian Hsp90 family of regulatory molecular chaperones. We show that maternally synthesized Hsp83 transcripts are localized to the posterior pole of the early Drosophila embryo by a novel mechanism involving a combination of generalized RNA degradation and local protection at the posterior. This protection of Hsp83 RNA occurs in wild-type embryos and embryos produced by females carrying the maternal effect mutations nanos and pumilio, which eliminate components of the posterior polar plasm without disrupting polar granule integrity. In contrast, Hsp83 RNA is not protected at the posterior pole of embryos produced by females carrying maternal mutations that disrupt the posterior polar plasm and the polar granules--cappuccino, oskar, spire, staufen, tudor, valois, and vasa. Mislocalization of oskar RNA to the anterior pole, which has been shown to result in induction of germ cells at the anterior, leads to anterior protection of maternal Hsp83 RNA. These results suggest that Hsp83 RNA is a component of the posterior polar plasm that might be associated with polar granules. In addition, we show that zygotic expression of Hsp83 commences in the anterior third of the embryo at the syncytial blastoderm stage and is regulated by the anterior morphogen, bicoid. We consider the possible developmental significance of this complex control of Hsp83 transcript distribution.

Additional Information

© 1993 by the American Society for Microbiology. Received 14 December 1992; returned for modification 20 January 1993; accepted 18 March 1993. We thank P. Lasko, T. Schupbach, A. Wohlwill, J. J. Bonner, H. Xiao, J. Lis, A. Ephrussi, R. Lehmann, and the Bowling Green and Indiana Drosophila Stock Centers for providing fly stocks; W. Fisher, J. Angus, and L. Richardson for technical assistance; E. Davidson for stimulating discussions about germ cell properties; and the following for critical comments on the manuscript: P. Sternberg, D. Weigel, K. Whittaker, and M. L. Yip. D.D. was supported in part by graduate fellowships from the California Foundation for Biochemical Research, the Lucille P. Markey Charitable Trust, and the Howard Hughes Medical Institute; S.M.P. was supported by a Developmental Biology Grant from the Lucille P. Markey Charitable Trust (to H.D.L.) and an NIH Developmental Biology Postdoctoral Training Grant Fellowship; S.R.H. was supported by an NIH Predoctoral Training Grant and a Markey Charitable Trust Predoctoral Fellowship. This research was supported by a U.S. Public Health Service Program Project Grant (GM40499) and an award from the Searle Scholars Program of the Chicago Community Trust (both to H.D.L.).

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