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Myc conquers all

Clones with extra dMyc (and extra GFP) greatly outgrow those with less dMyc (and no GFP). Basler/Elsevier

More Myc makes you stronger, according to Eduardo Moreno and Konrad Basler (Universität Zürich, Switzerland) and Claire de la Cova, Laura Johnston (Columbia University, New York, NY), and colleagues. They find that cell clones producing more dMyc overproliferate and outcompete their neighbors, with the neighbors dying off by apoptosis.

The concept of cell competition is not a new one. Fly cells mutant for various ribosomal proteins are known to suffer from competition-based elimination by wild-type cells. But now the two groups show that competition occurs in response to varying levels of the growth promoter dMyc, even when the "weaker" of the two cell groups are expressing wild-type levels of dMyc.

The Swiss group found that weaker cells could be rescued by either stimulating their rate of endocytosis (with an activated Rab5) or turning on genes downstream of the survival factor Dpp; outcompeted cells also had reduced expression of Dpp targets. Basler suggests weaker cells lose out because their lower metabolism is not driving a sufficiently robust endocytic cycle, leaving them with insufficient endocytosed survival factors.

But when it comes to Dpp, says Johnston, "we haven't been able to find any evidence." This colors her thinking of what the more competitive cells are doing. "We think they are not just sopping up nutritional and growth factors," she says. "We think there's a signal being sent" between cells of different metabolic capabilities.

The genesis and identity of such a signal remain unknown, but Johnston thinks it will connect competition to regulation of organ size. Her team found that fly wing discs repressed for apoptosis showed much greater variability in size than normal. They are currently testing whether this effect is based on competition or some other apoptosis-related phenomenon.

Basler remains skeptical of a connection to organ size. "We look at [competition] only as an artificial phenotype—at best it is an elimination plan for weak cells," he says. "It's more like a policeman—present but normally not needed." Where it might be important, he says, is in a stem cell niche where every cell must be a high performer. Incipient cancers may take advantage of this biology by expanding their domain at the expense of outcompeted normal cells.

References:

de la Cova, C., et al. 2004. Cell. 117:107–116.[CrossRef][Medline]

Moreno, E., and K. Basler. 2004. Cell. 117:117–129.[CrossRef][Medline]

William A. Wells

wellsw{at}rockefeller.edu

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This Article Full Text (PDF, 1420K) PPT slides of all figures Alert me when this article is cited Services Email this article Similar articles in this journal Alert me to new content in the JCB Download to citation manager Citing Articles Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Wells, W. A. Search for Related Content PubMed Articles by Wells, W. A. Social Bookmarking                            What's this?