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Published 9 July 2001. doi:10.1083/jcb1541rr2
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© The Rockefeller University Press, 0021-9525/2001/7/12-a $5.00
The Journal of Cell Biology, Volume 154, Number 1, July 9, 2001 12-a-12


Research Roundup

Algal Rb sets size limits


Multicellularity in Volvox may have arisen from Rb's cell cycle tricks.

David Kirk

A newly discovered Rb protein in the unicellular green alga Chlamydomonas reinhardtii sets a size limit for cell division, and may help explain how multicellularity evolved in algae such as Volvox.

Growth and division are uncoupled in Chlamydomonas cell cycles. During the day, cells remain in G1 to concentrate on photosynthesis, often growing to many times their original size. At night, however, cells undergo multiple alternating rounds of S phase and mitosis to produce 2n daughter cells.

Jim Umen and Ursula Goodenough of Washington University (St. Louis, MO) found that cells with a deletion in the mat3 gene of Chlamydomonas are smaller because of two perturbations in this cell cycle regimen. Mutant cells committed to entering a cell division cycle at a smaller than normal size, and those cells then underwent more than the usual number of rounds of DNA replication and division.

The gene at the mat3 locus encodes a protein that is very similar to mammalian Rb. This mammalian tumor suppressor restrains initiation of S phase when growth signals are absent. Mammalian Rb loss results in a shortened G1, whereas cells lacking mat3 retain their characteristically long G1, suggesting that the Chlamydomonas Rb pathway is not an S-phase switch, but a size sensor restraining cell cycle progression.

Umen notes that multicellular algal species often have 2n cells, suggesting that multicellularity arose when cells remained stuck together after a Chlamydomonas-style cell cycle. The Rb pathway, as the only Chlamydomonas pathway known to control cell size and the number of replication cycles, is a leading candidate for originally controlling the n in 2n. {blacksquare}



William A. Wells

wells{at}rockefeller.edu


References

Umen, J., and U. Goodenough. 2001. Genes Dev. 15:1652–1661.[Abstract/Free Full Text]


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