scholarly journals A MEIOTIC UV-SENSITIVE MUTANT THAT CAUSES DELETION OF DUPLICATIONS IN NEUROSPORA

Genetics ◽  
1978 ◽  
Vol 89 (2) ◽  
pp. 245-269
Author(s):  
Dorothy Newmeyer ◽  
Donna R Galeazzi
Keyword(s):  
Neurospora Crassa ◽  
Single Gene ◽  
Complete Loss ◽  
Duplicate Segment ◽  
Sensitive Mutant ◽  
Rearrangement Breakpoint ◽  
Ascospore Formation

ABSTRACT The meiotic-3 (mei-3) mutant of Neurospora crassa has several effects: (1) When homozygous, it almost completely blocks meiosis and ascospore formation, (2) it is sensitive to UV, (3) its growth is inhibited by histidine and, (4) it increases the instability of nontandem duplications. This was shown for duplications produced by five different rearrangements and was demonstrated by two different criteria. The effects on meiosis and duplication instability are expressed strongly at 25°; the effects on sensitivity to UV and to histidine are expressed strongly at 38.5° but only slightly at 25°. Nevertheless, all four effects were shown to be due to a single gene. mei-3 is not allelic with previously reported UV-sensitive mutants.—Two other results were obtained that are not necessarily due to mei-3: (1) A cross involving mei-3 produced a new unlinked meiotic mutant, mei-4, which is not sensitive to UV or histidine, and (2) a burst of several new mutants occurred in a different mei-3 stock, including a partial revertant of mei-3.—mei-3 has previously been shown to cause frequent complete loss of a terminal duplicate segment, beginning exactly at the original rearrangement breakpoint. Possible mechanisms are discussed by which a UV-sensitive mutant could cause such precise deletions.

scholarly journals A RECESSIVE CIRCADIAN CLOCK MUTATION AT THE frq LOCUS OF NEUROSPORA CRASSA

Genetics ◽  
1986 ◽  
Vol 114 (4) ◽  
pp. 1095-1110
Author(s):  
Jennifer J Loros ◽  
Adam Richman ◽  
Jerry F Feldman
Keyword(s):  
Circadian Clock ◽  
Neurospora Crassa ◽  
Temperature Compensation ◽  
Single Gene ◽  
Complete Loss ◽  
The Other ◽  
Compensation Mechanism ◽  
Wild Type ◽  
Structure Mapping ◽  
Clock Mutant

ABSTRACT A circadian clock mutant of Neurospora crassa, the most distinctive characteristic of which is the complete loss of temperature compensation of its period length, maps to the frq locus where seven other clock mutants have previously been mapped. This mutant, designated frq-9, is recessive to the wild-type allele and to each of the other frq mutants; thus, it differs from the other mutants, which show incomplete dominance to wild type and to each other. Complementation analysis suggests either that the frq locus is a single gene or that frq-9 is a deletion that overlaps adjacent genes. Preliminary efforts at fine structure mapping have indicated that recombination between certain pairs of frq mutations is less than 0.005%, a distance consistent with the locus being a single gene. The recessive nature of frq-9, coupled with complete loss of temperature compensation, suggests that this mutant may represent the null phenotype of the locus and that the frq gene is involved in the temperature compensation mechanism of the clock.—Genetic mapping studies have placed the frq locus on linkage group VIIR, midway between oli (oligomycin resistance) and for (formate auxotrophy), about 2 map units from each, and clearly indicate that frq and oli are separate genes.

scholarly journals DIRECT INDUCTION IN WILD-TYPE NEUROSPORA CRASSA OF MUTANTS (qa-1C) CONSTITUTIVE FOR THE CATABOLISM OF QUINATE AND SHIKIMATE

Genetics ◽  
1972 ◽  
Vol 72 (3) ◽  
pp. 411-417
Author(s):  
C W H Partridge ◽  
Mary E Case ◽  
Norman H Giles
Keyword(s):  
Neurospora Crassa ◽  
Single Gene ◽  
Ultra Violet ◽  
Wild Type ◽  
Color Test ◽  
Catabolic Enzymes ◽  
Direct Induction

ABSTRACT A color test has been developed for the selection and identification of mutants in Neurospora crassa, constitutive for the three normally inducible enzymes which convert quinate to protocatechuate. By this means seven such mutants have been recovered after ultra violet irradiation of wild type and have been shown to be allelic (or very closely linked) to the qa-1C mutants previously obtained by other means. Thus, the regulation of the synthesis of these three catabolic enzymes is indicated to be under the control of a single gene, qa-1+.

scholarly journals Identification and Characterization of Genes Required for Cell-to-Cell Fusion in Neurospora crassa

2011 ◽  
Vol 10 (8) ◽  
pp. 1100-1109 ◽  
Author(s):  
Ci Fu ◽  
Priyadarshini Iyer ◽  
Amrita Herkal ◽  
Julia Abdullah ◽  
Angela Stout ◽  
...  
Keyword(s):  
Signal Transduction ◽  
Transcription Factors ◽  
Neurospora Crassa ◽  
Cell Fusion ◽  
Single Gene ◽  
Vesicular Trafficking ◽  
Screening Procedure ◽  
Fusion Genes ◽  
Fusion Event ◽  
Screening Experiments

ABSTRACT A screening procedure was used to identify cell fusion (hyphal anastomosis) mutants in the Neurospora crassa single gene deletion library. Mutants with alterations in 24 cell fusion genes required for cell fusion between conidial anastomosis tubes (CATs) were identified and characterized. The cell fusion genes identified included 14 genes that are likely to function in signal transduction pathways needed for cell fusion to occur ( mik-1 , mek-1 , mak-1 , nrc-1 , mek-2 , mak-2 , rac-1 , pp2A , so/ham-1 , ham-2 , ham-3 , ham-5 , ham-9 , and mob3 ). The screening experiments also identified four transcription factors that are required for cell fusion ( adv-1 , ada-3 , rco-1 , and snf5 ). Three genes encoding proteins likely to be involved in the process of vesicular trafficking were also identified as needed for cell fusion during the screening ( amph-1 , ham-10 , pkr1 ). Three of the genes identified by the screening procedure, ham-6 , ham-7 , and ham-8 , encode proteins that might function in mediating the plasma membrane fusion event. Three of the putative signal transduction proteins, three of the transcription factors, the three putative vesicular trafficking proteins, and the three proteins that might function in mediating cell fusion had not been identified previously as required for cell fusion.

scholarly journals Isolation of Neurospora crassa A mating type mutants by repeat induced point (RIP) mutation.

Genetics ◽  
1992 ◽  
Vol 132 (1) ◽  
pp. 125-133 ◽  
Author(s):  
N L Glass ◽  
L Lee
Keyword(s):  
Neurospora Crassa ◽  
Mating Type ◽  
Single Copy ◽  
Open Reading Frame ◽  
Sexual Cycle ◽  
Reading Frame ◽  
Heterokaryon Incompatibility ◽  
Functional Regions ◽  
A Genome ◽  
Ascospore Formation

Abstract In the filamentous fungus, Neurospora crassa, mating type is regulated by a single locus with alternate alleles, termed A and a. The mating type alleles control entry into the sexual cycle, but during vegetative growth they function to elicit heterokaryon incompatibility, such that fusion of A and a hypha results in death of cells along the fusion point. Previous studies have shown that the A allele consists of 5301 bp and has no similarity to the a allele; it is found as a single copy and only within the A genome. The a allele is 3235 bp in length and it, too, is found as a single copy within the a genome. Within the A sequence, a single open reading frame (ORF) of 288 amino acids (mt A-1) is thought to confer fertility and heterokaryon incompatibility. In this study, we have used repeat induced point (RIP) mutation to identify functional regions of the A idiomorph. RIP mutations in mt A-1 resulted in the isolation of sterile, heterokaryon-compatible mutants, while RIP mutations generated in a region outside of mt A-1 resulted in the isolation of mutants capable of mating, but deficient in ascospore formation.

scholarly journals Characterization of Single Gene Deletion Mutants Affecting Alternative Oxidase Production in Neurospora crassa: Role of the yvh1 Gene

2020 ◽  
Vol 8 (8) ◽  
pp. 1186
Author(s):  
Adrien Beau Desaulniers ◽  
Nishka Kishore ◽  
Kelly Adames ◽  
Frank E. Nargang
Keyword(s):  
Neurospora Crassa ◽  
Gene Deletion ◽  
Alternative Oxidase ◽  
Single Gene ◽  
Ribosome Assembly ◽  
Mitochondrial Translation ◽  
Multiple Phenotypes ◽  
Transport Chain ◽  
Zinc Binding Domain ◽  
Single Gene Deletion

The Neurospora crassa AOD1 protein is a mitochondrial alternative oxidase that passes electrons directly from ubiquinol to oxygen. The enzyme is encoded by the nuclear aod-1 gene and is produced when the standard electron transport chain is inhibited. We previously identified eleven strains in the N. crassa single gene deletion library that were severely deficient in their ability to produce AOD1 when grown in the presence of chloramphenicol, an inhibitor of mitochondrial translation that is known to induce the enzyme. Three mutants affected previously characterized genes. In this report we examined the remaining mutants and found that the deficiency of AOD1 was due to secondary mutations in all but two of the strains. One of the authentic mutants contained a deletion of the yvh1 gene and was found to have a deficiency of aod-1 transcripts. The YVH1 protein localized to the nucleus and a post mitochondrial pellet from the cytoplasm. A zinc binding domain in the protein was required for rescue of the AOD1 deficiency. In other organisms YVH1 is required for ribosome assembly and mutants have multiple phenotypes. Lack of YVH1 in N. crassa likely also affects ribosome assembly leading to phenotypes that include altered regulation of AOD1 production.

scholarly journals Heat-sensitive mutant strain of Neurospora crassa, 4M(t), conditionally defective in 25S ribosomal ribonucleic acid production.

1981 ◽  
Vol 1 (3) ◽  
pp. 199-207 ◽  
Author(s):  
M W Loo ◽  
N S Schricker ◽  
P J Russell
Keyword(s):  
Neurospora Crassa ◽  
Mutant Strain ◽  
Ribosomal Rna ◽  
Ribonucleic Acid ◽  
Ribosomal Subunit ◽  
Macromolecular Synthesis ◽  
Sensitive Mutant ◽  
Ribosomal Subunits ◽  
Sequence Of Events ◽  
Ribosomal Rna Processing

A heat-sensitive mutant strain of Neurospora crassa, 4M(t), was studied in an attempt to define its molecular lesion. The mutant strain is inhibited in conidial germination and mycelial extension at the nonpermissive temperature (37 degrees C). Macromolecular synthesis studies showed that both ribonucleic acid (RNA) and protein syntheses are inhibited when 4-h cultures are shifted from 20 to 37 degrees C. Density gradient analysis of ribosomal subunits made at 37 degrees C indicated that strain 4M(t) is deficient in the accumulation of 60S ribosomal subunits in that the ratio of 60S/37S subunits was 0.29:1 compared with 1.6:1 for the parental strain. This phenotype was shown to be the result of a slow rate of processing of, and a deficiency in the amount of, the immediate precursor to 25S ribosomal RNA (the large RNA of the 60S subunit) in the sequence of events constituting the production of mature ribosomal RNAs from the primary transcript of the ribosomal deoxyribonucleic acid, the precursor ribosomal RNA molecule. Analysis of polysomes suggested that the heat-sensitive gene product might function in both the assembly and the function of the 60S ribosomal subunit, since there was a smaller proportion of newly made 60S subunits synthesized at 37 degrees C in the polysome region of the gradients than in the monosome-plus-subunit region. The ribosomal RNA processing defect is apparently responsible for the observed defects in germination and macromolecular synthesis at 37 degrees C, but the precise molecular lesion is not known. On the basis of these results, the heat-sensitive mutant allele in the 4M(t) strain is considered to define the rip1 (ribosome production) gene locus.

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