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Published online August 13, 2007
doi:10.1083/jcb.200704049
The Journal of Cell Biology, Vol. 178, No. 4, 661-673
The Rockefeller University Press, 0021-9525 $30.00
© 2007 Margalit et al.
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Article

Barrier to autointegration factor blocks premature cell fusion and maintains adult muscle integrity in C. elegans

Ayelet Margalit1, Esther Neufeld1, Naomi Feinstein1, Katherine L. Wilson2, Benjamin Podbilewicz3, and Yosef Gruenbaum1

1 Department of Genetics, The Institute of Life Sciences, The Hebrew University of Jerusalem, Givat Ram, Jerusalem 91904, Israel
2 Department of Cell Biology, Johns Hopkins University School of Medicine, Baltimore, MD 21205
3 Department of Biology, Technion-Israel Institute of Technology, Haifa 32000, Israel

Correspondence to Yosef Gruenbaum: gru{at}vms.huji.ac.il

Barrier to autointegration factor (BAF) binds double-stranded DNA, selected histones, transcription regulators, lamins, and LAP2–emerin–MAN1 (LEM) domain proteins. During early Caenorhabditis elegans embryogenesis, BAF-1 is required to organize chromatin, capture segregated chromosomes within the nascent nuclear envelope, and assemble lamin and LEM domain proteins in reforming nuclei. In this study, we used C. elegans with a homozygous deletion of the baf-1 gene, which survives embryogenesis and larval stages, to report that BAF-1 regulates maturation and survival of the germline, cell migration, vulva formation, and the timing of seam cell fusion. In the seam cells, BAF-1 represses the expression of the EFF-1 fusogen protein, but fusion still occurs in C. elegans lacking both baf-1 and eff-1. This suggests the existence of an eff-1–independent mechanism for cell fusion. BAF-1 is also required to maintain the integrity of specific body wall muscles in adult animals, directly implicating BAF in the mechanism of human muscular dystrophies (laminopathies) caused by mutations in the BAF-binding proteins emerin and lamin A.

Abbreviations list: BAF, barrier to autointegration factor; ChIP, chromatin immunoprecipitation; DIC, differential interference contrast; DTC, distal tip cell; LEM, LAP2–emerin–MAN1; VPC, vulval precursor cell.


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