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Published online before print April 2, 2007, 10.1101/gad.1516607
GENES & DEVELOPMENT 21:904-919, 2007
©2007 by Cold Spring Harbor Laboratory Press; ISSN 0890-9369/ $5.00
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Discovery of tMAC: a Drosophila testis-specific meiotic arrest complex paralogous to Myb–Muv B

Eileen L. Beall1,3, Peter W. Lewis1,3, Maren Bell1, Michael Rocha2, D. Leanne Jones2, and Michael R. Botchan1,4

1 Department of Molecular and Cell Biology, University of California, Berkeley, Berkeley, California 94720, USA; 2 The Salk Institute for Biological Studies, Laboratory of Genetics, La Jolla, California 92037, USA

The Drosophila Myb–Muv B (MMB)/dREAM complex regulates gene expression and DNA replication site-specifically, but its activities in vivo have not been thoroughly explored. In ovarian amplification-stage follicle cell nuclei, the largest subunit, Mip130, is a negative regulator of replication, whereas another subunit, Myb, is a positive regulator. Here, we identified a mutation in mip40 and generated a mutation in mip120, two additional MMB subunits. Both mutants were viable, but mip120 mutants had many complex phenotypes including shortened longevity and severe eye defects. mip40 mutant females had severely reduced fertility, whereas mip120 mutant females were sterile, substantiating ovarian regulatory role(s) for MMB. Myb accumulation and binding to polytene chromosomes was dependent on the core factors of the MMB complex. In contrast to the documented mip130 mutant phenotypes, both mip40 and mip120 mutant males were sterile. We purified Mip40-containing complexes from testis nuclear extracts and identified tMAC, a new testis-specific meiotic arrest complex that contained Mip40, Caf1/p55, the Mip130 family member, Always early (Aly), and a Mip120 family member, Tombola (Tomb). Together, these data demonstrate that MMB serves diverse roles in different developmental pathways, and members of MMB can be found in alternative, noninteracting complexes in different cell types.

[Keywords: Drosophila; Myb–Muv B; replication; spermatid differentiation; chorion amplification]

Received November 27, 2006; revised version accepted February 27, 2007.


3 These authors contributed equally to this work.

4 Corresponding author.

E-MAIL mbotchan{at}uclink4.berkeley.edu; FAX (510) 643-1729.

Supplemental material is available at http://www.genesdev.org.

Article published online ahead of print. Article and publication date are online at http://www.genesdev.org/cgi/doi/10.1101/gad.1516607


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