drosophila rbp6 is an orthologue of vertebrate msi-1 and msi-2, but does not function redundantly with dmsi to regulate germline stem cell behaviour果蝇rbp6是脊椎动物的一个orthologue msi-1 msi-2,但不与dmsi功能多余地调节生殖系干细胞的行为.pdfVIP
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drosophila rbp6 is an orthologue of vertebrate msi-1 and msi-2, but does not function redundantly with dmsi to regulate germline stem cell behaviour果蝇rbp6是脊椎动物的一个orthologue msi-1 msi-2,但不与dmsi功能多余地调节生殖系干细胞的行为
Drosophila Rbp6 Is an Orthologue of Vertebrate Msi-1
and Msi-2, but Does Not Function Redundantly with
dMsi to Regulate Germline Stem Cell Behaviour
1,2 1,2 1 1,2 1
Nicole A. Siddall , Marina Kalcina , Timothy M. Johanson , Adrian C. Monk , Franca Casagranda ,
Reeva P. Been1, Eileen A. McLaughlin2,3, Gary R. Hime1,2*
1 Anatomy and Neuroscience, University of Melbourne, Parkville, Australia, 2 ARC Centre of Excellence in Biotechnology and Development, Callaghan, Australia, 3 School
of Environmental and Life Science, University of Newcastle, Callaghan, Australia
Abstract
The vertebrate RNA-binding proteins, Musashi-1 (Msi-1) and Musashi-2 (Msi-2) are expressed in multiple stem cell
populations. A role for Musashi proteins in preventing stem cell differentiation has been suggested from genetic analysis of
the Drosophila family member, dMsi, and both vertebrate Msi proteins function co-operatively to regulate neural stem cell
behaviour. Here we have identified a second Drosophila Msi family member, Rbp6, which shares more amino acid identity
with vertebrate Msi-1 and Msi-2 than dMsi. We generated an antibody that detects most Rbp6 splice isoforms and show that
Rbp6 is expressed in multiple tissues throughout development. However, Rbp6 deletion mutants generated in this study are
viable and fertile, and show only minor defects. We used Drosophila spermatogonial germline stem cells (GSC’s) as a model
to test whether Drosophila Msi proteins function redundantly to regulate stem cell behaviour. However, like vertebrate Msi-
1 and Msi-2, Rbp6 and Msi do not appear to be co-expressed in spermatogenic GSC’s and do not function co-operatively in
the regulation of GSC main
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