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© The Rockefeller University Press, 0021-9525/1998//1321 $5.00
The Journal of Cell Biology, Volume 140, Number 6, , 1998 1321-1329

Article

ncl-1 Is Required for the Regulation of Cell Size and Ribosomal RNA Synthesis in Caenorhabditis elegans



Deborah J. Frank and Mark B. Roth

Division of Basic Sciences and Molecular and Cellular Biology Program, Fred Hutchinson Cancer Research Center, Seattle, Washington 98109

Regulation of ribosome synthesis is an essential aspect of growth control. Thus far, little is known about the factors that control and coordinate these processes. We show here that the Caenorhabditis elegans gene ncl-1 encodes a zinc finger protein and may be a repressor of RNA polymerase I and III transcription and an inhibitor of cell growth. Loss of function mutations in ncl-1, previously shown to result in enlarged nucleoli, result in increased rates of rRNA and 5S RNA transcription and enlarged cells. Furthermore, ncl-1 adult worms are larger, have more protein, and have twice as much rRNA as wild-type worms. Localization studies show that the level of NCL-1 protein is independently regulated in different cells of the embryo. In wild-type embryos, cells with the largest nucleoli have the lowest level of NCL-1 protein. Based on these results we propose that ncl-1 is a repressor of ribosome synthesis and cell growth.

Abbreviations used in this paper: ITS, internal transcribed spacer; PML, promyelocytic leukemia; RAR, retinoic acid receptor; Rb, retinoblastoma gene; UTP, uridine 5'triphosphate.

D.J. Frank was supported by a graduate fellowship from the National Science Foundation. This work was supported by a National Institutes of Health grant (GM48435-01A2) to M.B. Roth.

Address all correspondence to Mark B. Roth, Fred Hutchinson Cancer Research Center, 1100 Fairview Ave., N Mailstop A3-013, Seattle, WA 98109. Tel.: (206) 667-5602. Fax: (206) 667-6877. E-mail: mroth{at}fred.fhcrc.org


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