A mutant gene that disrupts growth and reproduction of the basidiomycete fungus Schizophyllum commune was first discovered and described by Leonard (1975). The name mnd was given to this gene because the mutation causes dense, rounded masses of hyphae (hyphal mounds) to form on fungal colonies. This recessive mutant allele uses an enigmatic molecular mechanism that seems to transfer heritable genetic information to partner nuclei in dikaryotic cells, replacing the original information. From a morphological standpoint, an allele of a pheromone receptor-like gene, prl1, was previously implicated in the development of mounds in strain HK28. A PCR assay of mound-producing colonies for the prl1 allele shows its presence was not essential for monokaryotic mound formation. By placing mnd- and Δku80 in the same genome, it was also shown that monokaryotic mound formation and the underlying mechanism initiating it occurs in mnd- strains lacking canonical nonhomologous end-joining repair. Previous genetic maps link ade2 to mnd, so the location of ade2 was identified in the most recent genome assembly of S. commune (H4-8) to tie the genetic and physical maps of S. commune together. A fosmid library of mnd- strain HK28 genomic DNA was constructed that covers the S. commune genome 4.24 times and has a 98.6% probability of including any particular gene sequence. A fosmid containing ade2 was isolated from the genomic library. DNA sequence from the fosmid insert’s ends confirmed the ade2 gene and surrounding region is located centrally on Scaffold 1 of the genome sequence. This successful PCR screen informs and anchors a walk or skip from ade2 towards mnd in the genome of S. commune.
|Commitee:||DiSalvo, Susanne, Petruccelli, Emily|
|School:||Southern Illinois University at Edwardsville|
|School Location:||United States -- Illinois|
|Source:||MAI 58/06M(E), Masters Abstracts International|
|Subjects:||Biology, Molecular biology, Genetics|
|Keywords:||Ade2, Fosmid, Hyphae, Mnd, Morphogenesis, Schizophyllum commune|
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