The Genetic Basis of Homology Recognition in Coprinus Cinereus

University Of North Carolina At Chapel Hill, Chapel Hill NC

Investigators

Abstract

The mechanisms responsible for meiotic chromosome pairing, and their relationship to genetic recombination, are not understood. Several mutants that disrupt pairing and synapsis in defined ways have been isolated in previous work from this laboratory. None of the mutants affects the repair of DNA damage induced by ionizing radiation. Analysis of double mutant phenotypes has revealed that these genes do not appear to act in a simple linear pathway. In addition to disrupting meiotic pairing (as assayed by microscopy and in situ hybridization), some of these mutants also affect the epigenetic modification of duplicated DNA sequences. Accordingly, epistasis analysis will be used to ask if five additional synaptic mutants (including spo11, which blocks the initiation of meiotic recombination) can be incorporated into the two previously defined genetic pathways. Relationships between chromosome pairing and recombination early in meiotic prophase will be analyzed using in situ hybridization and PCR. Epistatic interactions among mutants exhibiting defects in the recognition and methylation of DNA duplications will be examined. Finally, a combination of methods will be used to obtain cloned DNA sequences that can complement the defects in duplication-dependent DNA methylation and/or synapsis conferred by three synaptic mutants (bad45, bad48, and bad42). In conclusion, this research will use a unique collection of mutants with well-characterized defects in DNA and chromosome pairing to determine cause and effect relationships among these processes that are essential to maintain genome stability.