For yeast, a DNA break ensures sex switch for a grandchild

November 08, 2004

New work has established a molecular mechanism to explain how fission yeast cells manage to switch the mating type of a certain proportion of individuals over the course of two generations. This genetic trick has been long studied but poorly understood. Researchers now report that yeast achieve the switch by enacting a special kind of programmed DNA break at a specific genomic site that controls mating type, the yeast equivalent of gender.

When yeast cells divide, their progeny receive the same genomic DNA, yet the fate of the cells of the next generation will not be identical. One of the two daughter cells will produce a granddaughter cell that has switched its sexual mating type. Two decades ago, researchers proposed that a chromosomal imprint at the mating-type locus was responsible for generating two rounds of asymmetric division. Now Benoit Arcangioli's group at the Pasteur Institute in Paris, France, has identified a new imprinting mechanism that controls sexual switching in yeast.

The French group has now demonstrated that the genomic DNA at the mating-type locus of the yeast Schizosaccharomyces pombe is marked by a simple break on one strand of the DNA. One of the daughter cells will receive this nicked DNA upon cell division, and the nick serves as a signal for sex switching in the next generation. The researchers showed that the nick is site specific but sequence independent. The single-strand break is protected by 3'-OH and 5'-OH modification of the two DNA ends, and there is not loss of nucleotides.

In their new work, the authors propose that this represents the first example of an imprinting event that is due to a simple single-strand break. The discovery has general implications for how DNA can be marked for asymmetric inheritance that can affect cell destiny.
Atanas Kaykov and Benoit Arcangioli: "A Programmed Strand-Specific and Modified Nick in S. pombe Constitutes a Novel Type of Chromosomal Imprint"

Publishing in Current Biology, Volume 14, Number 21, November 9, 2004, pages 1924-1928.

Cell Press

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