Spore Killer Research Articles

Genetics of Gibberella fujikuroi V. Spore killer alleles in G. fujikuroi

A spore killer phenomenon is described ma plant parasitic fungus, Gibberella fujikuroi var. subglutinans Spore killer (SKk) spore sensitive (SKk) and partially spore killer-sensitive (SKmx) alleles exist side by side in natural populations of this fungus. The pi-operties of these alleles are similar to those found in Fusarium monillforme and Neurospora sitophila.

SPORE KILLER POLYMORPHISM IN FUSARIUM MONILIFORME

A Spore killer trait, which exhibits genetic and cytological properties analogous to those previously found in Neurospora, exists in natural populations of the fungal plant pathogen Fusarium moniliforme. The genogeography of the polymorphism in F. moniliforme differs from the situation in Neurospora intermedia. It is more akin to the situation in N. sitophila, although more extreme with respect to the prevalence of killer alleles: more than 80% of tested isolates of F. moniliforme carry the killer allele. Nevertheless, sensitive alleles are widely distributed and have been found in California, Italy, Greece and Central America.

Genetic organization of the mouse t complex

The mouse t complex (also known as the T locus or T/t complex) is a large region of chromosome 17 that has intrigued geneticists for more than 50 years with its striking and unorthodox features. These include suppression of recombination, disturbances of embryonic development and alterations of sperm differentiation and function. Much of our knowledge concerning the properties of this genetic complex is based on the early work performed by S. Gluecksohn Waelsch and L. C. Dunn with mutant forms of the t complex called t haplotypes (previously known as t alleles or t mutations). Many t haplotypes are characterized by lethal actions at particular stages during early embryogenesis. Lethal t haplotypes can be placed into a number of groups where members of each group do not complement each other. Complementation between t haplotypes of different groups is not complete, and prenatal death occurs in many, but not all, doubly heterozygous (V/t”) embryos. Furthermore, all males doubly heterozygous for two lethal haplotypes are completely sterile. Other genes defined separately from t haplotypes but mapping within the t complex include Brachyury (T), Kinky (Fuk’) and Knobbly (Fukb), which are recessive embryonic lethals; Hybrid sterility-l (Hst-7) and Quaking (qk), which cause male-specific sterility; Hye, which affects the level of male-specific H-Y antigen expression; and Gtl, which determines acceptance or rejection specifically of embryonal carcinoma cell grafts. All observations to date imply a crucial role for the t complex in mechanisms of development and differentiation. At the present time, however, the molecular events responsible for these t complex effects remain elusive. This review will therefore focus on recent advances in our understanding of the structure, rather than the function, of this region. All known t haplotypes originated from wild populations, and almost all wild mouse populations analyzed from around the world have been found to be polymorphic for lethal or semi-lethal t haplotypes. Maintenance of a deleterious gene in a wild population is unexpected, but can be accounted for in this case by a further property of t haplotypes called transmission-ratio distortion (also known as segregation distortion). A wild heterozygous (+/t) male can transmit his t haplotype to more than 95% of his offspring, and it appears that the advantage of the t haplotype at fertilization can overcome the disadvantage of a certain frequency of homozygous lethality in the population as a whole. Genetic systems that involve the maintenance of deleterious gene complexes in wild populations by transmission-ratio distortion have been identified in other well studied species, and include the SD complex of Drosophila melanogaster, and the Spore Killer (SK) complex in Neurospora (Turner and Minireviews

The mutation SK(ad-3A) cancels the dominance of ad-3A+ over ad-3A in the ascus of Neurospora.

A newly induced mutant of Neurospora, when crossed with an ad-3A mutant, produces asci with four viable black and four inviable white ascospores. The survivors always contain the new mutant allele, never ad-3A. The new allele, which is called SK(ad-3A) (for spore killer of ad-3A), is located at or very near the ad-3A locus.--In crosses homozygous for ad-3A, each ascus contains only inviable white ascospores. This defect in ascospore maturation is complemented by the wild-type allele, ad-3A+ (crosses heterozygous for ad-3A and ad-3A+ produce mainly viable ascospores), but it is not complemented by the new SK(ad-3A) allele (all ad-3A ascospores from crosses heterozygous for SK(ad-3A) and ad-3A are white and inviable). In crosses homozygous for SK(ad-3A) or heterozygous for SK(ad-3A) and ad-3A+, each ascus contains only viable black ascospores. SK(ad-3A) does not require adenine for growth, and forced heterokaryons between SK(ad-3A) and ad-3A grow at wild-type rates and produce conidia of both genotypes with approximately equal frequency. Thus, the action of SK(ad-3A) is apparently restricted to ascospore formation. Possible mechanisms of the action of this new allele are discussed.

SPORE KILLER, A CHROMOSOMAL FACTOR IN NEUROSPORA THAT KILLS MEIOTIC PRODUCTS NOT CONTAINING IT

Three chromosomal factors called Spore killer (Sk) have been found in wild populations of Neurospora sitophila and N. intermedia. Sk resembles other examples of meiotic drive such as Segregation Distorter in Drosophila, Pollen killer in wheat, and Gamete eliminator in tomato. In crosses heterozygous for Sk, each ascus contains four viable black ascospores and four inviable, undersize, clear ascospores, with second-division segregations infrequent. The survivors contain the killer allele Sk(K), while unlinked markers segregate normally. Reciprocal crosses are identical. When crosses are homozygous for an allele of Sk, all eight ascospores are viable and black in most asci. (Many homozygous crosses have a background level of randomly occurring inviable spores; however, the pattern of 4 viable: 4 small clear ascospores is not found in any of the asci of Sk-homozygous crosses.)--Killer (Sk-1(K)) and sensitive (Sk-1(S)) alleles occur in about equal numbers among a worldwide sample of N. sitophila strains, following no geographic pattern. No killer allele has been found in N. crassa. Sk-2(K) and Sk-3(K), found in N. intermedia, are rare. Most N. intermedia strains are Sk-2(S) and Sk-3(S), but some are wholly or partially resistant to one or both of the killer alleles, while not themselves acting as killers. Sk-2(K) and Sk-2(R) are both specific in conferring resistance to Sk-2(K), but not to Sk-3(K). Likewise Sk-3(K) and Sk-3(R) are resistant specifically to Sk-3(K), but not to Sk-2(K). Resistance segregates as an allele of Sk(K).--Sk-2 and Sk-3 have been mapped near the centromere of linkage group III after introgression into N. crassa, where crossing over is normally 11% between the proximal III markers acr-2 and leu-1. But crossing over is absent in this region when either of the killer alleles is heterozygous (Sk-2(K)xSk-2(S), Sk-3(K)xSk-3(S) and Sk-2(K)xSk-2(R) have been examined).

CYTOGENETIC BEHAVIOR OF SPORE KILLER GENES IN NEUROSPORA

Crosses heterozygous and homozygous for Sk-1, Sk-2 and Sk-3 were examined by light microscopy. All three Spore killers behave similarly. In heterozygous killer x sensitive crosses, meiosis and ascospore development are normal until after the second postmeiotic mitosis when four of the eight ascospores in each ascus stop developing and degenerate. The four surviving ascospores carry the killer. Death of sensitives thus occurs only after killer and sensitive alleles, Sk(K) and Sk(S), have segregated into separate ascospores. Homozygous killer x killer crosses do not show such a pattern of degeneration. Either all ascospores are normal or, if some fail to mature, they do not resemble the degenerating sensitive ascospores in heterozygous asci.--With Sk-2, it was shown that Sk(S) nuclei do not abort when both Sk(K) and Sk(S) are present in the same ascospore. Mutants affecting ascus development were used to obtain large ascospores enclosing both Sk(K) and Sk(S) meiotic products in a common cytoplasm. Sk(S) nuclei do not then undergo the degeneration that would be seen if they were sequestered into separate ascospores, and viable Sk(S) progeny are recovered in undiminished numbers when the mixed multinucleate large ascospores are germinated. In a four-spored mutant, where each ascospore encloses a single nucleus following meiosis, degeneration of Sk(S) ascospores nevertheless occurs, even though the third nuclear division is omitted. Cycloheximide and temperature treatments do not affect the expression of Sk(K).