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Genetics and Genomics

Victor R. Ambros

Cell Cycle

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Full-Text Articles in Life Sciences

Prb/Cki Pathways At The Interface Of Cell Cycle And Development, Victor Ambros Oct 2015

Prb/Cki Pathways At The Interface Of Cell Cycle And Development, Victor Ambros

Victor R. Ambros

Comment on: The cyclin-dependent kinase inhibitors, cki-1 and cki-2, act in overlapping but distinct pathways to control cell-cycle quiescence during C. elegans development. Buck SH, et al. Cell Cycle 2009; 8:2613-20.


The Temporal Control Of Cell Cycle And Cell Fate In Caenorhabditis Elegans, Victor Ambros Dec 2000

The Temporal Control Of Cell Cycle And Cell Fate In Caenorhabditis Elegans, Victor Ambros

Victor R. Ambros

The nematode Caenorhabditis elegans develops through two major phases: the first phase, embryogenesis, consists of a rapid series of cleavage cell divisions leading to morphogenesis of a first stage larva. The second phase is postembryonic development, which consists of developmentally regulated cell cycles that occur during the four larval stages leading to the adult. Precursor cells set aside during embryogenesis divide through stereotypical cell lineage patterns during the four larval stages to generate larval and adult structures. The precise timing of the postembryonic cell divisions is under strict control, in most cases with a developmentally regulated G1. In certain postembryonic …


Cell Cycle-Dependent Sequencing Of Cell Fate Decisions In Caenorhabditis Elegans Vulva Precursor Cells, Victor Ambros Apr 1999

Cell Cycle-Dependent Sequencing Of Cell Fate Decisions In Caenorhabditis Elegans Vulva Precursor Cells, Victor Ambros

Victor R. Ambros

In Caenorhabditis elegans, the fates of the six multipotent vulva precursor cells (VPCs) are specified by extracellular signals. One VPC expresses the primary (1 degrees ) fate in response to a Ras-mediated inductive signal from the gonad. The two VPCs flanking the 1 degrees cell each express secondary (2 degrees ) fates in response to lin-12-mediated lateral signaling. The remaining three VPCs each adopt the non-vulval tertiary (3 degrees ) fate. Here I describe experiments examining how the selection of these vulval fates is affected by cell cycle arrest and cell cycle-restricted lin-12 activity. The results suggest that lin-12 participates …


Developmental Regulation Of A Cyclin-Dependent Kinase Inhibitor Controls Postembryonic Cell Cycle Progression In Caenorhabditis Elegans, Yang Hong, Richard Roy, Victor Ambros Aug 1998

Developmental Regulation Of A Cyclin-Dependent Kinase Inhibitor Controls Postembryonic Cell Cycle Progression In Caenorhabditis Elegans, Yang Hong, Richard Roy, Victor Ambros

Victor R. Ambros

C. elegans cki-1 encodes a member of the CIP/KIP family of cyclin-dependent kinase inhibitors, and functions to link postembryonic developmental programs to cell cycle progression. The expression pattern of cki-1::GFP suggests that cki-1 is developmentally regulated in blast cells coincident with G1, and in differentiating cells. Ectopic expression of CKI-1 can prematurely arrest cells in G1, while reducing cki-1 activity by RNA-mediated interference (RNAi) causes extra larval cell divisions, suggesting a role for cki-1 in the developmental control of G1/S. cki-1 activity is required for the suspension of cell cycling that occurs in dauer larvae and starved L1 larvae in …


Heterochronic Genes Control Cell Cycle Progress And Developmental Competence Of C. Elegans Vulva Precursor Cells, Susan Euling, Victor Ambros Mar 1996

Heterochronic Genes Control Cell Cycle Progress And Developmental Competence Of C. Elegans Vulva Precursor Cells, Susan Euling, Victor Ambros

Victor R. Ambros

Heterochronic genes control the timing of vulval development in the C. elegans hermaphrodite. lin-14 or lin-28 loss-of-function mutations cause the vulval precursor cells (VPCs) to enter S phase and to divide one larval stage earlier than in the wild type. A precocious vulva is formed by essentially normal cell lineage patterns, governed by the same intercellular signals as in the wild type. Mutations that prevent the normal developmental down-regulation of lin-14, activity delay or block VPC division and prevent vulval differentiation. A genetic pathway that includes lin-4, lin-14, and lin-28 controls when VPCs complete G1 and also controls when VPCs …