Role ofAdducin-like (hu-li tai shao) mRNA and protein localization in regulating cytoskeletal structure and function duringDrosophila oogenesis and early embryogenesis
✍ Scribed by Zaccai, Michèle ;Lipshitz, Howard D.
- Book ID
- 102660666
- Publisher
- John Wiley and Sons
- Year
- 1996
- Tongue
- English
- Weight
- 895 KB
- Volume
- 19
- Category
- Article
- ISSN
- 0192-253X
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✦ Synopsis
Adducin is a cytoskeletal protein that can function in vitro to bundle F-actin and to control the assembly of the F-actidspectrin cytoskeletal network. We previously reported cloning of the Drosophila Adducin-like (Add) locus [Ding ef a/., 19931 also referred to as hu-li fai shao (hisf [Yue and Spradling, 19921, and identification of two adducin-related protein isoforms: a 95 x lo3 M, form (ADD-95) and an 87 x lo3 M, form (ADD-87) [Zaccai and Lipshitz, 19961. ADD-87 protein is present throughout the oocyte cortex at stages 9 and 10 of oogenesis but is restricted to its anterior pole from stage 11 onward. This ADD-87 protein localization is preceded by localization of Add-hts mRNA first to the cortex and then to the anterior pole of the oocyte. Mutation of the swallow gene results in delocalization of Add-hfs mRNA and ADD-87 protein from the cortex of stage 9 and 10 oocytes, and from the anterior pole of later stage oocytes. Early embryos produced by swallow or Add-hts mutant females have severe defects in the distribution of F-actin and spectrin as well CIS abnormalities in nuclear division, nuclear migration, and cellularization. In addition to their cytoskeletal defects, embryos produced by swallow females have an abnormal anterior pattern be- cause bicoid mRNA is delocalized from the anterior pole. In contrast, bicoid mRNA is still found at the anterior of embryos produced by Add-hfs mothers. Thus swallow functions to restrict bicoid mRNA and Add-hts mRNA to the cortex of the oocyte. Cortical restriction of Add-hfs mRNA and protein is required for the normal structure and function of the early embryonic F-actidspeckin cytoskeleton. A defective embryonic cytoskeleton can be induced in either of two ways: (1) by delocalization of functional ADD from the oocyte cortex (as in swallow mutants), or (2) by reduction of ADD function while retaining its normal cortical localization during oogenesis (as in Add-hfs mutants).