Send to

Choose Destination
See comment in PubMed Commons below
Genetics. 2010 Aug;185(4):1271-82. doi: 10.1534/genetics.110.117184. Epub 2010 Jun 2.

Meiotic regulators Ndt80 and ime2 have different roles in Saccharomyces and Neurospora.

Author information

Department of Plant and Microbial Biology, University of California, Berkeley, California 94720, USA.


Meiosis is a highly regulated process in eukaryotic species. The filamentous fungus Neurospora crassa has been shown to be missing homologs of a number of meiotic initiation genes conserved in Saccharomyces cerevisiae, but has three homologs of the well-characterized middle meiotic transcriptional regulator NDT80. In this study, we evaluated the role of all three NDT80 homologs in the formation of female reproductive structures, sexual development, and meiosis. We found that none of the NDT80 homologs were required for meiosis and that even the triple mutant was unaffected. However, strains containing mutations in NCU09915 (fsd-1) were defective in female sexual development and ascospore maturation. vib-1 was a major regulator of protoperithecial development in N. crassa, and double mutants carrying deletions of both vib-1 (NCU03725) and fsd-1 exhibited a synergistic effect on the timing of female reproductive structure (protoperithecia) formation. We further evaluated the role of the N. crassa homolog of IME2, a kinase involved in initiation of meiosis in S. cerevisiae. Strains containing mutations in ime-2 showed unregulated development of protoperithecia. Genetic analysis indicated that mutations in vib-1 were epistatic to ime-2, suggesting that IME-2 may negatively regulate VIB-1 activity. Our data indicate that the IME2/NDT80 pathway is not involved in meiosis in N. crassa, but rather regulates the formation of female reproductive structures.

[Indexed for MEDLINE]
Free PMC Article
PubMed Commons home

PubMed Commons

How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for HighWire Icon for PubMed Central
    Loading ...
    Support Center