SEXUAL ORIGINS OF BRITISH ASPERGILLUS-NIDULANS ISOLATES

Citation
Dm. Geiser et al., SEXUAL ORIGINS OF BRITISH ASPERGILLUS-NIDULANS ISOLATES, Proceedings of the National Academy of Sciences of the United Statesof America, 91(6), 1994, pp. 2349-2352
Citations number
25
Categorie Soggetti
Multidisciplinary Sciences
ISSN journal
00278424
Volume
91
Issue
6
Year of publication
1994
Pages
2349 - 2352
Database
ISI
SICI code
0027-8424(1994)91:6<2349:SOOBAI>2.0.ZU;2-P
Abstract
Aspergillus nidulans is a holomorphic fungus, capable of producing bot h meiotically and mitotically derived spores. Meiosis may be an evolut ionary relic in this species because it is potentially capable of mito tic recombination and because most Aspergilli lack the ability to prod uce meiotic spores. We tested the null hypothesis that meiosis has bee n a major factor in the origin of strains of A. nidulans from Great Br itain by estimating linkage disequilibrium among restriction fragment length polymorphisms. These strains belong to different heterokaryon c ompatibility groups and are thus incapable of undergoing mitotic recom bination with one another, so any recombination evidenced by linkage e quilibrium is assumed to be the result of meiosis. Eleven cosmid clone s of known chromosomal origin were used to generate multilocus genotyp es based on restriction-pattern differences for each heterokaryon comp atibility group. Low levels of genetic variation and little linkage di sequilibrium were found, indicating that the heterokaryon compatibilit y groups represent recently diverged lineages that arose via meiotic r ecombination. The null hypothesis that loci are independent could not be rejected. Additionally, low levels of electrophoretic karyotype var iation were indicative of meiosis. We conclude that although A. nidula ns probably propagates in a primarily clonal fashion, recombination ev ents are frequent enough to disrupt the stable maintenance of clonal g enotypes. We further conclude that the British heterokaryon compatibil ity groups arose via recombination and not through novel mutation.