Huang, Linda S. and Tzou, Phoebe and Sternberg, Paul W. (1994) The lin-15 locus encodes two negative regulators of Caenorhabditis elegans vulval development. Molecular Biology of the Cell, 5 (4). pp. 395-412. ISSN 1059-1524 http://resolver.caltech.edu/CaltechAUTHORS:HUAmbc94
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During Caenorhabditis elegans vulval development, an inductive signal from the anchor cell stimulates three of the six vulval precursor cells (VPCs) to adopt vulval rather than nonvulval epidermal fates. Genes necessary for this induction include the lin-3 growth factor, the let-23 receptor tyrosine kinase, and let-60 ras. lin-15 is a negative regulator of this inductive pathway. In lin-15 mutant animals, all six VPCs adopt vulval fates, even in the absence of inductive signal. Previous genetic studies suggested that lin-15 is a complex locus with two independently mutable activities, A and B. We have cloned the lin-15 locus by germline transformation and find that it encodes two nonoverlapping transcripts that are transcribed in the same direction. The downstream transcript encodes the lin-15A function; the upstream transcript encodes the lin-15B function. The predicted lin-15A and lin- 15B proteins are novel and hydrophilic. We have identified a molecular null allele of lin-15 and have used it to analyze the role of lin-15 in the signaling pathway. We find that lin-15 acts upstream of let-23 and in parallel to the inductive signal.
|Additional Information:||Copyright © 1994 by The American Society for Cell Biology Submitted December 21, 1993; Accepted February 7, 1994. Monitoring Editor: Judith Kimble We are greatly indebted to the generosity of Min Han, Jane Mendel, and Russell Hill for assistance with the microinjections; Jane Mendel for isolating PS#74B3; Andrea Holboke for help in mapping the lin-15 region; Alan Coulson for numerous discussions and assistance with correlating the physical and genetic maps around lin-15, Monica Driscoll and Marty Chalfie for TU#W1723; Mike Nonet and Barbara Meyer for communicating the cloning of sdc-1 before publication; Mimi Sengupta for help with the lin-15B(n744) mutagenesis; Tom Blumenthal for discussions regarding SL2 trans-splicing; Junho Lee for lin-15A(syl97); Russell Hill for lin-15AB(n767sy222); the Horvitz lab for lin-36B(n766) and the lin-15 alleles n765, n377, n309, el 763, and nl 139; Chris Martin, Stuart Kim, and Bob Barstead for cDNA libraries; and Paul Garrity for hints on LMPCR and gifts of primers LMPCR.1 and LMPCR.2. We are grateful to Helen Chamberlin, Tom Clandinin, Paul Garrity, Wendy Katz, Andy Golden, Yvonne Hajdu, Paul Kayne, and Bino Palmer for critically reading this manuscript. Some nematode strains used in this study were provided by the Caenorhabditis Genetics Center, which is funded by the National Institutes of Health (NIH) National Center for Research Resources. This work was supported by a grant from the March of Dimes Birth Defects Foundation to P.W.S. and NIH award GM-07616 to L.S.H. P.W.S. is an investigator of the Howard Hughes Medical Institute.|
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|Deposited On:||18 Jul 2006|
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