Originally published as Genetics Published Articles Ahead of Print on July 14, 2005.

Genetics, Vol. 171, 1017-1031, November 2005, Copyright © 2005
doi:10.1534/genetics.104.034173

lin-8, Which Antagonizes Caenorhabditis elegans Ras-Mediated Vulval Induction, Encodes a Novel Nuclear Protein That Interacts With the LIN-35 Rb Protein

Ewa M. Davison^*, Melissa M. Harrison^*, Albertha J. M. Walhout^,1, Marc Vidal and H. Robert Horvitz^*,2

^* Department of Biology, Howard Hughes Medical Institute, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139 and Dana-Farber Cancer Institute and Department of Genetics, Harvard Medical School, Boston, Massachusetts 02115

² Corresponding author: Department of Biology, Howard Hughes Medical Institute, Room 68-425, Massachusetts Institute of Technology, 77 Massachusetts Ave., Cambridge, MA 02139.
E-mail: horvitz{at}mit.edu

Ras-mediated vulval development in C. elegans is inhibited by the functionally redundant sets of class A, B, and C synthetic Multivulva (synMuv) genes. Three of the class B synMuv genes encode an Rb/DP/E2F complex that, by analogy with its mammalian and Drosophila counterparts, has been proposed to silence genes required for vulval specification through chromatin modification and remodeling. Two class A synMuv genes, lin-15A and lin-56, encode novel nuclear proteins that appear to function as a complex. We show that a third class A synMuv gene, lin-8, is the defining member of a novel C. elegans gene family. The LIN-8 protein is nuclear and can interact physically with the product of the class B synMuv gene lin-35, the C. elegans homolog of mammalian Rb. LIN-8 likely acts with the synMuv A proteins LIN-15A and LIN-56 in the nucleus, possibly in a protein complex with the synMuv B protein LIN-35 Rb. Other LIN-8 family members may function in similar complexes in different cells or at different stages. The nuclear localization of LIN-15A, LIN-56, and LIN-8, as well as our observation of a direct physical interaction between class A and class B synMuv proteins, supports the hypothesis that the class A synMuv genes control vulval induction through the transcriptional regulation of gene expression.

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