Note: When clicking on a Digital Object Identifier (DOI) number, you will be taken to an external site maintained by the publisher.
Some full text articles may not yet be available without a charge during the embargo (administrative interval).
What is a DOI Number?
Some links on this page may take you to non-federal websites. Their policies may differ from this site.
-
Free, publicly-accessible full text available October 2, 2026
-
Free, publicly-accessible full text available September 9, 2026
-
Free, publicly-accessible full text available August 1, 2026
-
Free, publicly-accessible full text available January 1, 2026
-
Meiotic recombination between homologous chromosomes is vital for maximizing genetic variation among offspring. However, sex-determining regions are often rearranged and blocked from recombination. It remains unclear whether rearrangements or other mechanisms might be responsible for recombination suppression. Here, we uncover that the deficiency of the DNA cytosine methyltransferase DNMT1 in the green algaChlamydomonas reinhardtiicauses anomalous meiotic recombination at the mating-type locus (MT), generating haploid progeny containing bothplusandminusmating-type markers due to crossovers withinMT. The deficiency of a histone methyltransferase for H3K9 methylation does not lead to anomalous recombination. These findings suggest that DNA methylation, rather than rearrangements or histone methylation, suppresses meiotic recombination, revealing an unappreciated biological function for DNA methylation in eukaryotes.more » « less
An official website of the United States government
