The A mating-type genes of the mushroom Coprinus cinereus are not differentially transcribed in monokaryons and dikaryons

1993 ◽  
Vol 238-238 (1-2) ◽  
pp. 304-307 ◽  
Author(s):  
Wendy V. J. Richardson ◽  
Ursula Kues ◽  
Lorna A. Casselton
1993 ◽  
Vol 241-241 (3-4) ◽  
pp. 474-478 ◽  
Author(s):  
Michael P. Challen ◽  
Timothy J. Elliott ◽  
Ursula Kües ◽  
Lorna A. Casselton

Genetics ◽  
1998 ◽  
Vol 149 (4) ◽  
pp. 1753-1761 ◽  
Author(s):  
Yukio Murata ◽  
Motohiro Fujii ◽  
Miriam E Zolan ◽  
Takashi Kamada

Abstract A homokaryotic strain (5337) in our culture stock of Coprinus cinereus produced fertile fruit bodies after prolonged culture. Microscopic examination revealed that hyphae dedifferentiated from the tissues of one of the fruit bodies, as well as all basidiospore derivatives from the fruit body, exhibited pseudoclamps, whereas vegetative hyphae of 5337, from which the fruit body developed, had no clamp connections. Genetic analysis showed that the formation of pseudoclamps results from a recessive mutation in a gene designated pcc1 (pseudoclamp connection formation), which is distinct from the A and B mating type genes. Cloning and sequencing of the pcc1 gene and cDNA identified an ORF of 1683 bp interrupted by one intron. Database searches revealed that pcc1 encodes an SRY-type HMG protein. The HMG box shared 44, 41, and 29% sequence identities (>80 amino acids) to those of FPR1 of Podospora anserina, MAT-Mc of Schizosaccharomyces pombe, and prf1 of Ustilago maydis, respectively. Northern analysis revealed that the level of pcc1 expression is higher in the dikaryon, in homokaryons in which the A and B mating type developmental sequences are individually activated, than in the homokaryon in which these sequences are not active. Sequencing of the pcc1-1 mutant allele revealed that the mutant carries a nonsense mutation at serine 211, a residue located between the HMG box and the C terminus. Based on these results, possible roles of the pcc1 gene in the sexual development of homobasidiomycetes are discussed.


Genetics ◽  
1996 ◽  
Vol 144 (4) ◽  
pp. 1437-1444
Author(s):  
C Ian Robertson ◽  
Kirk A Bartholomew ◽  
Charles P Novotny ◽  
Robert C Ullrich

The Aα locus is one of four master regulatory loci that determine mating type and regulate sexual development in Schizophyllum commune. We have made a plasmid containing a URA1 gene disruption of the Aα Y1 gene. Y1 is the sole Aα gene in Aα1 strains. We used the plasmid construction to produce an Aα null (i.e., AαΔ) strain by replacing the genomic Y1 gene with URA1 in an Aα1 strain. To characterize the role of the Aα genes in the regulation of sexual development, we transformed various Aα Y and Z alleles into AαΔ strains and examined the acquired mating types and mating abilities of the transformants. These experiments demonstrate that the Aα Y gene is not essential for fungal viability and growth, that a solitary Z Aα mating-type gene does not itself activate development, that Aβ proteins are sufficient to activate the A developmental pathway in the absence of Aα proteins and confirm that Y and Z genes are the sole determinants of Aα mating type. The data from these experiments support and refine our model of the regulation of A-pathway events by Y and Z proteins.


2003 ◽  
Vol 40 (1) ◽  
pp. 25-37 ◽  
Author(s):  
R.S Bennett ◽  
S.-H Yun ◽  
T.Y Lee ◽  
B.G Turgeon ◽  
E Arseniuk ◽  
...  

1986 ◽  
Vol 6 (2) ◽  
pp. 688-702 ◽  
Author(s):  
J M Ivy ◽  
A J Klar ◽  
J B Hicks

Mating type in the yeast Saccharomyces cerevisiae is determined by the MAT (a or alpha) locus. HML and HMR, which usually contain copies of alpha and a mating type information, respectively, serve as donors in mating type interconversion and are under negative transcriptional control. Four trans-acting SIR (silent information regulator) loci are required for repression of transcription. A defect in any SIR gene results in expression of both HML and HMR. The four SIR genes were isolated from a genomic library by complementation of sir mutations in vivo. DNA blot analysis suggests that the four SIR genes share no sequence homology. RNA blots indicate that SIR2, SIR3, and SIR4 each encode one transcript and that SIR1 encodes two transcripts. Null mutations, made by replacement of the normal genomic allele with deletion-insertion mutations created in the cloned SIR genes, have a Sir- phenotype and are viable. Using the cloned genes, we showed that SIR3 at a high copy number is able to suppress mutations of SIR4. RNA blot analysis suggests that this suppression is not due to transcriptional regulation of SIR3 by SIR4; nor does any SIR4 gene transcriptionally regulate another SIR gene. Interestingly, a truncated SIR4 gene disrupts regulation of the silent mating type loci. We propose that interaction of at least the SIR3 and SIR4 gene products is involved in regulation of the silent mating type genes.


1990 ◽  
Vol 10 (1) ◽  
pp. 409-412 ◽  
Author(s):  
G P Livi ◽  
J B Hicks ◽  
A J Klar

The silent mating-type genes (HML and HMR) of Saccharomyces cerevisiae are kept under negative transcriptional control by the trans-acting products of the four MAR/SIR loci. MAR/SIR gene mutations result in the simultaneous derepression of HML and HMR gene expression. The sum1-1 mutation was previously identified as an extragenic suppressor of mutations in MAR1 (SIR2) and MAR2 (SIR3). As assayed genetically, sum1-1 is capable of restoring repression of silent mating-type information in cells containing mar1 or mar2 null mutations. We show here that the mating-type phenotype associated with sum1-1 results from a dramatic reduction in the steady-state level of HML and HMR gene transcripts. At the same time, the sum1-1 mutation has no significant effect on the level of each of the four MAR/SIR mRNAs.


1993 ◽  
Vol 104 (2) ◽  
pp. 227-230
Author(s):  
U. Kues ◽  
L.A. Casselton

Having multiple mating types greatly improves the chances of meeting a compatible mating partner, particularly in an organism like the mushroom that has no sexual differentiation and no mechanism for signalling to a likely mate. Having several thousands of mating types, as some mushrooms do, is, however, remarkable - and even more remarkable is the fact that individuals only recognise that they have met a compatible mate after their cells have fused. How are such large numbers of mating types generated and what is the nature of the intracellular interaction that distinguishes self from non- self? Answers to these fascinating questions come from cloning some of the mating type genes of the ink cap mushroom Coprinus cinereus. A successful mating in Coprinus triggers a major switch in cell type, the conversion of a sterile mycelium with uninucleate cells (monokaryon) to a fertile mycelium with binucleate cells (dikaryon) which differentiates the characteristic fruit bodies. The mating type genes that regulate this developmental switch map to two multiallelic loci designated A and B and these must both carry different alleles for full mating compatibility. A and B independently regulate different steps in the developmental switch, making it possible to study just one component of the system and work in our laboratory has concentrated on understanding the structure and function of the A genes. It is estimated that some 160 different A mating types exist in nature, any two of which can together trigger the A-regulated part of sexual development. The first clue to how such large numbers are generated came from classical genetic analysis, which identified two functionally redundant A loci, (alpha) and beta. Functional redundancy is, indeed, the key to multiple A mating types and, as seen in Fig.1, molecular cloning has identified many more genes than was possible by recombination analysis.


1989 ◽  
Vol 9 (11) ◽  
pp. 4621-4630
Author(s):  
D J Mahoney ◽  
J R Broach

Mating-type genes resident in the silent cassette HML at the left arm of chromosome III are repressed by the action of four SIR gene products, most likely mediated through two cis-acting sites located on opposite sides of the locus. We showed that deletion of either of these two cis-acting sites from the chromosome did not yield any detectable derepression of HML, while deletion of both sites yielded full expression of the locus. In addition, each of these sites was capable of exerting repression of heterologous genes inserted in their vicinity. Thus, HML expression is regulated by two independent silencers, each fully competent for maintaining repression. This situation was distinct from the organization of the other silent locus, HMR, at which a single silencer served as the predominant repressor of expression. Examination of identifiable domains and binding sites within the HML silencers suggested that silencing activity can be achieved by a variety of combinations of various functional domains.


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