The cell type ofRhodosporidium toruloides after protoplast fusion between strains of identical and opposite mating type

1983 ◽  
Vol 9 (5) ◽  
pp. 297-300 ◽  
Author(s):  
Dietmar Becher ◽  
Fritz Böttcher

Genetics ◽  
1993 ◽  
Vol 134 (4) ◽  
pp. 1045-1054 ◽  
Author(s):  
G Thon ◽  
A J Klar

Abstract Cells of homothallic strains of Schizosaccharomyces pombe efficiently switch between two mating types called P and M. The phenotypic switches are due to conversion of the expressed mating-type locus (mat1) by two closely linked silent loci, mat2-P and mat3-M, that contain unexpressed information for the P and M mating types, respectively. In this process, switching-competent cells switch to the opposite mating type in 72-90% of the cell divisions. Hence, mat2-P is a preferred donor of information to mat1 in M cells, whereas mat3-M is a preferred donor in P cells. We investigated the reason for the donor preference by constructing a strain in which the genetic contents of the donor loci were swapped. We found that switching to the opposite mating type was very inefficient in that strain. This shows that the location of the silent cassettes in the chromosome, rather than their content, is the deciding factor for recognition of the donor for each cell type. We propose a model in which switching is achieved by regulating accessibility of the donor loci, perhaps by changing the chromatin structure in the mating-type region, thus promoting an intrachromosomal folding of mat2 or mat3 onto mat1 in a cell type-specific fashion. We also present evidence for the involvement of the Swi6 and Swi6-mod trans-acting factors in the donor-choice mechanism. We suggest that these factors participate in forming the proposed folded structure.



2011 ◽  
Vol 10 (6) ◽  
pp. 753-760 ◽  
Author(s):  
Song Yi ◽  
Nidhi Sahni ◽  
Karla J. Daniels ◽  
Kevin L. Lu ◽  
Guanghua Huang ◽  
...  

ABSTRACTLikeMTL-heterozygous (a/α) cells, whiteMTL-homozygous (a/aor α/α) cells ofCandida albicans, to which a minority of opaque cells of opposite mating type have been added, form thick, robust biofilms. The latter biofilms are uniquely stimulated by the pheromone released by opaque cells and are regulated by the mitogen-activated protein kinase signal transduction pathway. However, whiteMTL-homozygous cells, to which opaque cells of opposite mating type have not been added, form thinner biofilms. Mutant analyses reveal that these latter biofilms are self-induced. Self-induction ofa/abiofilms requires expression of the α-receptor geneSTE2and the α-pheromone geneMFα, and self-induction of α/α biofilms requires expression of thea-receptor geneSTE3and thea-pheromone geneMFa. In both cases, deletion ofWOR1, the master switch gene, blocks cells in the white phenotype and biofilm formation, indicating that self-induction depends upon low frequency switching from the white to opaque phenotype. These results suggest a self-induction scenario in which minority opaquea/acells formed by switching secrete, in a mating-type-nonspecific fashion, α-pheromone, which stimulates biofilm formation through activation of the α-pheromone receptor of majority whitea/acells. A similar scenario is suggested for a white α/α cell population, in which minority opaque α/α cells secretea-pheromone. This represents a paracrine system in which one cell type (opaque) signals a second highly related cell type (white) to undergo a complex response, in this case the formation of a unisexual white cell biofilm.



Genetics ◽  
1986 ◽  
Vol 113 (3) ◽  
pp. 601-619
Author(s):  
Karen P VanWinkle-Swift ◽  
Jang-Hee Hahn

ABSTRACT The non-Mendelian erythromycin resistance mutation ery-u1 shows bidirectional uniparental inheritance in crosses between homothallic ery-u1 and ery-u1  + strains of Chlamydomonas monoica. This inheritance pattern supports a general model for homothallism invoking intrastrain differentiation into opposite compatible mating types and, further, suggests that non-Mendelian inheritance is under mating-type (mt) control in C. monoica as in heterothallic species. However, the identification of genes expressed or required by one gametic cell type, but not the other, is essential to verify the existence of a regulatory mating-type locus in C. monoica and to understand its role in cell differentiation and sexual development. By screening for a shift from bidirectional to unidirectional transmission of the non-Mendelian ery-u1 marker, a mutant with an apparent mating-type-limited sexual cycle defect was obtained. The responsible mutation, mtl-1, causes a 1000-fold reduction in zygospore germination in populations homozygous for the mutant allele and, approximately, a 50% reduction in germination for heterozygous (mtl-1/mtl-1  +) zygospores. By next screening for strains unable to yield any viable zygospores in a cross to mtl-1, a second putative mating-type-limited mutant, mtl-2, was obtained. The mtl-2 strain, although self-sterile, mates efficiently with mtl-2  + strains and shows a unidirectional uniparental pattern of inheritance for the ery-u1 cytoplasmic marker, similar to that observed for crosses involving mtl-1. Genetic analysis indicates that mtl-1 and mtl-2 define unique unlinked Mendelian loci and that the sexual cycle defects of reduced germination (mtl-1) or self-sterility (mtl-2) cosegregate with the effect on ery-u1 cytoplasmic gene transmission. By analogy to C. reinhardtii, the mtl-1 and mtl-2 phenotypes can be explained if the expression of these gene loci is limited to the mt  + gametic cell type, or if the wild-type alleles at these loci are required for the normal formation and/or functioning of mt  + gametes only.



1975 ◽  
Vol 17 (3) ◽  
pp. 441-449 ◽  
Author(s):  
A. M. DeLange ◽  
A. J. F. Griffiths

In Neurospora crassa, strains of opposite mating type generally do not form stable heterokaryons because the mating type locus acts as a heterokaryon incompatibility locus. However, when one A and one a strain, having complementing auxotrophic mutants, are placed together on minimal medium, growth may occur, although the growth is generally slow. In this study, escape from such slow growth to that at a wild type or near-wild type rate was observed. The escaped cultures are stable heterokaryons, mostly having lost the mating type allele function from one component nucleus, so that the nuclear types are heterokaryon compatible. Either A or a mating type can be lost. This loss of function has been attributed to deletion since only one nuclear type could be recovered in all heterokaryons except one, but deletion spanning adjacent loci has been directly demonstrated in a minority of cases. Alternatively when one component strain is tol and the other tol+ (tol being a recessive mutant suppressing the heterokaryon incompatibility associated with mating type), escape may occur by the deletion or mutation of tol+, also resulting in heterokaryon compatibility. An induction mechanism for escape is speculated upon.



1989 ◽  
Vol 12 (3-4) ◽  
pp. 211-217 ◽  
Author(s):  
D.N. Shah ◽  
K.S. Sriprakash ◽  
B.B. Chattoo


Cell ◽  
1983 ◽  
Vol 32 (2) ◽  
pp. 409-415 ◽  
Author(s):  
George F. Sprague ◽  
Robert Jensen ◽  
Ira Herskowitz




1987 ◽  
Vol 7 (9) ◽  
pp. 3185-3193
Author(s):  
K Inokuchi ◽  
A Nakayama ◽  
F Hishinuma

The MF alpha 1 gene of Saccharomyces cerevisiae, a major structural gene for mating pheromone alpha factor, is an alpha-specific gene whose expression is regulated by the mating-type locus. To study the role of sequences upstream of MF alpha 1 in its expression and regulation, we generated two sets of promoter deletions: upstream deletions and internal deletions. By analyzing these deletions, we have identified a TATA box and two closely related, tandemly arranged upstream activation sites as necessary elements for MF alpha 1 expression. Two upstream activation sites were located ca. 300 and 250 base pairs upstream of the MF alpha 1 transcription start points, which were also determined in this study. Each site contained a homologous 22-base-pair sequence, and both sites were required for maximum transcription level. The distance between the upstream activation sites and the transcription start points could be altered without causing loss of transcription efficiency, and the sites were active in either orientation with respect to the coding region. These elements conferred cell type-specific expression on a heterologous promoter. Analysis with host mating-type locus mutants indicates that these sequences are the sites through which the MAT alpha 1 product exerts its action to activate the MF alpha 1 gene. Homologous sequences with these elements were found in other alpha-specific genes, MF alpha 2 and STE3, and may mediate activation of this set of genes by MAT alpha 1.



Mycologia ◽  
1999 ◽  
Vol 91 (5) ◽  
pp. 858-870 ◽  
Author(s):  
Y. Anikster ◽  
T. Eilam ◽  
L. Mittelman ◽  
L.J. Szabo ◽  
W. R. Bushnell


1990 ◽  
Vol 10 (5) ◽  
pp. 2247-2260 ◽  
Author(s):  
S Y Roth ◽  
A Dean ◽  
R T Simpson

The yeast alpha 2 repressor suppresses expression of a-mating-type-specific genes in haploid alpha and diploid a/alpha cell types. We inserted the alpha 2-binding site into the multicopy TRP1/ARS1 yeast plasmid and examined the effects of alpha 2 on the chromatin structure of the derivative plasmids in alpha cells, and a/alpha cells. Whereas no effect on nucleosome position was observed in a cells, nucleosomes were precisely and stably positioned over sequences flanking the alpha 2 operator in alpha and a/alpha cells. In addition, when the alpha 2 operator was located upstream of the TRP1 gene, an extended array of positioned nucleosomes was formed in alpha cells and a/alpha cells, with formation of a nucleosome not present in a cells, and TRP1 mRNA production was substantially reduced. These data indicate that alpha 2 causes a positioning of nucleosomes over sequences proximal to its operator in TRP1/ARS1 chromatin and suggest that changes in chromatin structure may be related to alpha 2 repression of cell-type-specific genes.



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