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| Image from Hochwagen Lab |
This proposal was shouted
out as “…one of the most important papers on the control of meiotic
crossing over…” (Hawley 2006). Since then, “homeostasis” has been offered
as the explanation for a variety of observations that demonstrate a degree of
independence of crossover frequency (and sometimes crossover interference) from
the frequency of double-strand breaks. As in the original yeast work, none of
these papers questions whether “homeostasis” has anything to recommend it as an
explanation because none has addressed the mundane possibility that crossover
constancy reflects merely the normal operation of the system, rather than a
reaction to a perceived aberration.
Without trying to explore the universe of
alternate explanations for “homeostasis” in this Blog, we offer just one simple
one, based on the view that the crossover/noncrossover “decision” is made
“early”, either before or at the onset of the period of double-strand-breaks
(Storlazzi et al. 1996): In this none-too-original model, the first double-strand
break to occur on a chromosome is immediately assigned to the pathway that
leads to crossing over, accounting for both the “obligate crossover” (Jones and
Franklin 2006) and the preservation of crossing over. Additional
double-strand-breaks are directed to become crossovers when they meet the
conditions imposed by crossover interference. [It appears notable that
Drosophila, which clearly lacks an “obligate crossover”, has also shown no
evidence of “homeostasis” (Stahl 2008).]
This blogger would
like to be informed of any “homeostasis” data for which such a nonhomeostatic
explanation fails.
LITERATURE CITED
Chen, S. Y., T. Tsubouchi, B. Rockmill, J. S. Sandler, D. R.
Richards et al., 2008 Global analysis of the meiotic crossover
landscape. Dev. Cell 15: 401–415.
Hawley, R. S.,
2006 "This is one of the most
important papers on the control of meiotic crossing over..." Evaluation
of: [Martini et al.,
2006 Crossover homeostasis in yeast
meiosis. Cell 126: 285-295; doi:
10.1016/j.cell.2006.05.044]. Faculty of 1000, 14 Aug 2006.
F1000.com/1033723#eval387934
Henderson, K. A., and S. Keeney,
2004 Tying synaptonemal complex
initiation to the formation and programmed repair of DNA double-strand breaks. Proc. Natl. Acad. Sci. USA 101: 4519–4524.
Jones, G. H., and F. C.
Franklin, 2006 Meiotic crossing-over: obligation and interference. Cell 126: 246–248.
Martini, E., R. L. Diaz, N.
Hunter and S. Keeney, 2006 Crossover
homeostasis in yeast meiosis. Cell 126:
285-295.
Martini, E., V. Borde, M.
Legendre, S. Audic, B. Regnault et al.,
2011 Genome-wide analysis of
heteroduplex DNA in mismatch repair-deficient yeast cells reveals novel
properties of meiotic recombination pathways. PLoS Genet. 7: e1002305.
Mehrotra, S. and K. S. McKim,
2006 Temporal analysis of meiotic DNA
double-strand break formation and repair in Drosophila females. PLoS Genetics 2: 1883-1897.
Stahl,
F. W., 2008 Countdown with Mehrotra and
McKim. Online comment on Mehrotra and McKim (2006) 2(11): e200
doi:10.1371/journal.pgen.0020200.
Storlazzi, A., L. Xu, A.
Schwacha and N. Kleckner, 1996 Synaptonemal complex (SC) component Zip1 plays a
role in meiotic recombination independent of SC polymerization along the
chromosomes. Proc. Natl. Acad. Sci. USA 93: 9043–9048.
Molecular Biology
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Eugene, OR 97403-1229
