Genetics. Published Articles Ahead of Print: June 4, 2006, Copyright © 2006
doi:10.1534/genetics.106.057562


A more recent version of this article appeared on August 1, 2006.

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A nonself recognition gene complex in Neurospora crassa

Cristina O Micali 1 and Myron L Smith 2*

1 Max-Planck Institute for Plant Breeding Research
2 Carleton University

* To whom correspondence should be addressed. E-mail: mysmith{at}ccs.carleton.ca.

Submitted on February 23, 2006
Revised on March 23, 2006
Accepted on 30 May 2006


Abstract

Nonself recognition is exemplified in the fungal kingdom by the regulation of cell fusion events between genetically different individuals (heterokaryosis). The het-6 locus is one of about ten that controls heterokaryon incompatibility during vegetative growth of N. crassa. Previously, it was found that het-6-associated incompatibility in Oak Ridge (OR) strains involves two linked genes, het-6 and un-24. The OR allele of either gene causes "strong" incompatibility (cell death) when transformed into Panama (PA)-background strains. Several remarkable features of the locus include the nature of these incompatibility genes (het-6 is a member of a repetitive gene family and un-24 also encodes the large subunit of ribonucleotide reductase) and the observation that un-24 and het-6 are in severe linkage disequilibrium. Here, we identify "weak" (slow, aberrant growth) incompatibility activities by un-24PA and het-6PA when transformed separately into OR strains, whereas together they exhibit an additive, strong effect. We synthesized strains with the combinations un-24PA het-6OR and un-24OR het-6PA that are not found in nature and found that these strains grow normally and have distinct nonself recognition capabilities but may have reduced fitness. Comparing the Oak Ridge and Panama het-6 regions revealed a paracentric inversion, the architecture of which provides insights into the evolution of the un-24-het-6 gene complex.

Key Words: balancing selection, heterokaryon incompatibility, inversion polymorphism, linkage disequilibrium, ribonucleotide reductase




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