Ascus development in two temperature-sensitive Four-spore mutants of Neurospora crassa

1986 ◽  
Vol 28 (6) ◽  
pp. 982-990 ◽  
Author(s):  
Namboori B. Raju

Two nonallelic Four-spore mutants are known in which ascospore walls enclose the four immediate products of meiosis rather than the normal eight products of a postmeiotic mitosis. Expression depends on temperature. The Four-spore phenotype is expressed when the developing asci are subjected either to high temperatures (25–30 °C) for Fsp-1 or to low temperatures (15–20 °C) for Fsp-2. Heterozygous Fsp-1 × Fsp-1+ crosses make eight-spored asci at 15–20 °C but produce many four-spored asci at 25 °C and mostly four-spored asci at 30 °C. Homozygous Fsp-1 × Fsp-1 crosses respond similarly to increasing temperature but make 40–50% four-spored asci even at 20 °C. Heterozygous Fsp-2 × Fsp-2+ crosses produce almost exclusively four-spored asci at 15 °C but a mixture of four- and eight-spored asci at 20, 25, and 30 °C. Homozygous Fsp-2 × Fsp-2 crosses make all four-spored asci at 15 and 20 °C and a mixture of four- and eight-spored asci at 25 and 30 °C. When both Fsp-1 and Fsp-2 are present in a cross, either homozygous or heterozygous, no asci contain more than four ascospores at any temperature. Limited temperature-shift experiments with Fsp-1 and Fsp-2 show that the sensitive period for Four-spore expression is sometime after meiotic prophase, possibly at interphase II.Key words: Neurospora, temperature sensitive, Four-spore mutants, large ascospores.

1994 ◽  
Vol 357 ◽  
Author(s):  
Witold Lojkowski ◽  
Bogdan Palosz

AbstractThe aim of the paper is to explain the recently observed de-wetting grain boundary transition with increasing temperature. On the example of a bicrystal from the Fe-6at.%Si alloy, it was found recently that as temperature is increased, the following GB transitions take place: “solid” (or regular) GB-→“premelted” GB →“solid” GB. At the same time the wetting/de-wetting transitions have taken place. Another example of such GB behavior was discovered during sintering of alumina. The inverse melting behavior is explained as follows: low melting point impurities cause GB premelting at low temperatures, However de-segregation of impurities at high temperatures causes return of the GB structure to its regular “solid” state.


Genetics ◽  
1981 ◽  
Vol 97 (3-4) ◽  
pp. 581-606 ◽  
Author(s):  
Donald A R Sinclair ◽  
David T Suzuki ◽  
Thomas A Grigliatti

ABSTRACT A temperature-sensitive (ts) third chromosome Minute (M) mutation, designated Q-III, has been recovered and characterized. Q-III heterozygotes raised at 29" exhibit all of the dominant traits of M mutants including small bristles, rough eyes, prolonged development, reduced viability 2nd interactions with several unrelated mutations. Q-III homozygotes raised at 29° are lethal; death occurs primarily during the first larval instar. When raised at 22°, Q-Ill heterozygotes are phenotypically normal and Q-III homozygotes display moderate Mtraits. In addition, Q-IIIelicits ts sterility and maternal-effect lethality. As it true of Mlesions, the dominant traits of Q-111 are not expressed in triploid females raised at 29°. Complementation tests suggest that Q-III is a ts allele of M(3)LS4, which is located in 3L near the centromere.——Reciprocal temperature-shift experiments revealed that the temperature-sensitive period (TSP) of Q-111 lethality is polyphasic, extending from the first instar to the latter half of pupation. Heat-pulse experiments further resolved this into two post-embryonic TSPs: one occurring during the latter half of the second larval instar, and the other extending from the larval/pupal boundary to the second half of pupation. In addition, heat pulses elicited a large number of striking adult phenotypes in Q-III individuals. These included pattern alterations such as deficiencies and duplications and cther morphological defects in structures produced by the eye-antennal, leg, wing and genital imaginal discs and the abdominal histoblasts. Each defect or pattern alteration is associated with a specific TSP during development.——We favor the interpretation that most of the major Q-III defects, particularly the structural duplications and deficiencies, result from temperature-induced cell death in mitotically active imaginal anlagen, while the small macrochaete phene probably results from the direct effects of Q-III on bristle synthesis. The hypothesis that the Q-III locus specifices a component required for protein synthesis is discussed, and it is concluded that this hypothesis can account for the pleiotropy of Q-III, and that perhaps it can be extended to M loci in general.


Genetics ◽  
1988 ◽  
Vol 118 (1) ◽  
pp. 61-74
Author(s):  
T M Rogalski ◽  
D L Riddle

Abstract The amanitin-binding subunit of RNA polymerase II in Caenorhabditis elegans is encoded by the ama-1 gene, located approximately 0.05 map unit to the right of dpy-13 IV. Using the amanitin-resistant ama-1(m118) strain as a parent, we have isolated amanitin-sensitive mutants that carry recessive-lethal ama-1 alleles. Of the six ethyl methanesulfonate-induced mutants examined, two are arrested late in embryogenesis. One of these is a large deficiency, mDf9, but the second may be a novel point mutation. The four other mutants are hypomorphs, and presumably produce altered RNA polymerase II enzymes with some residual function. Two of these mutants develop into sterile adults at 20 degrees but are arrested as larvae at 25 degrees, and two others are fertile at 20 degrees and sterile at 25 degrees. Temperature-shift experiments performed with the adult sterile mutant, ama-1(m118m238ts), have revealed a temperature-sensitive period that begins late in gonadogenesis and is centered around the initiation of egg-laying. Postembryonic development at 25 degrees is slowed by 30%. By contrast, the amanitin-resistant allele of ama-1 has very little effect on developmental rate or fertility. We have identified 15 essential genes in an interval of 4.5 map units surrounding ama-1, as well as four gamma-ray-induced deficiencies and two duplications that include the ama-1 gene. The larger duplication, mDp1, may include the entire left arm of chromosome IV, and it recombines with the normal homologue at a low frequency. The smallest deficiency, mDf10, complements all but three identified genes: let-278, dpy-13 and ama-1, which define an interval of only 0.1 map unit. The terminal phenotype of mDf10 homozygotes is developmental arrest during the first larval stage, suggesting that there is sufficient maternal RNA polymerase II to complete embryonic development.


1967 ◽  
Vol 105 (1) ◽  
pp. 39-44 ◽  
Author(s):  
D J Bennett ◽  
E H Creaser

Amino acid changes in the enzyme l-histidinol dehydrogenase (l-histidinol–NAD oxidoreductase, EC 1.1.1.23) have been determined between the wild-type Neurospora crassa and two temperature-sensitive mutants. Comparison was made between amino acid analyses of peptides of differing electrophoretic and chromatographic mobilities resulting from tryptic and chymotryptic digestion of protein from wild-type and mutant K26, and wild-type and mutant K445 strains, respectively. The analyses demonstrate the substitution of aspartic acid for alanine in mutant K26, and leucine for histidine in mutant K445. The effects of the resulting changes in polarity and charge are discussed in relation to the catalytic functioning of the proteins.


1987 ◽  
Vol 88 (2) ◽  
pp. 241-250
Author(s):  
LAI-WA TAM ◽  
STEPHEN F. NG

Reduction in the length of the oral apparatus produced by the temperature-sensitive mutation short-1 (sh1) involved suppressed growth of the oral primordium in all stages of development. Temperature shift-up and heat-shock experiments revealed that the temperature-sensitive period of this mutation coincided with nearly the entire stomatogenic phase (stages 1–6) in sexual reproduction. Low- and high-sensitivity phases were noted, corresponding to the periods of slow (stages 1 and 2) and rapid (stage 3 to stage 6) elongation of the oral primordium, respectively. The action of sh1 is thus concentrated after stage 2. The mutation hypothetically results in defective membrane growth and extension in the oral primordium, leading to restriction in incorporation of basal bodies into the developing membranelles.


1981 ◽  
Vol 38 (3) ◽  
pp. 297-314 ◽  
Author(s):  
John C. Sparrow

SUMMARYThe recovery of two EMS induced mutations which are dominant suppressors of the lethality of cryptocephal in Drosophila melanogaster are described. One of these mutations Su(crc)1 is described in detail. It maps very close to cryptocephal at 54·7 on the second chromosome and its suppression of cryptocephal is temperature-sensitive. Temperature shift experiments show that the temperature-sensitive period is from before the pupariation until 12 h post pupariation. The temperature-sensitive period of Su(crc)1 is discussed in relation to the expression of l(2)crc, head eversion and the timing of pupal chitin synthesis.


Genetics ◽  
1975 ◽  
Vol 79 (4) ◽  
pp. 613-634
Author(s):  
W J Peacock ◽  
George L Gabor Miklos ◽  
D J Goodchild

ABSTRACT The meiotic drive characteristics of the In(1)sc4Lsc8R/Y system have been examined by genetic analysis and by light and electron microscopy. sc4sc8/Y males show a direct correlation between nondisjunction frequency and meiotic drive. Temperature-shift experiments reveal that the temperature-sensitive period for nondisjunction is at meiosis, whereas that for meiotic drive has both meiotic and post-meiotic components. Cytological analyses in the light and electron microscopes reveal failures in spermiogenesis in the testes of sc  4  sc  8 males. The extent of abnormal spermatid development increases as nondisjunction becomes more extreme.


Genetics ◽  
1994 ◽  
Vol 137 (3) ◽  
pp. 829-836 ◽  
Author(s):  
P N Adler ◽  
J Charlton ◽  
W J Park

Abstract The adult cuticular wing of Drosophila is covered with an array of distally pointing hairs. Mutations in the inturned (in) gene result in both abnormal hair polarity (i.e., hairs no longer point distally), and, in most cells forming more than one hair. We have isolated and characterized a collection of in alleles. Among this collection of alleles are a number of rearrangements that enable us to assign in to 77B3-5. Almost all of the in alleles, including putative null alleles, result in a stronger phenotype on the wing at 18 degrees than 29 degrees. The data argue that the in-dependent process is cold-sensitive. Temperature shift experiments with a hypomorphic allele show that this cold sensitivity can be relieved by several hours of incubation at the permissive temperature at a variety of times in the early pupae, but that this ability ends prior to the start of hair morphogenesis. One new allele showed a dramatic heat sensitivity. Temperature shift experiments with this allele revealed a very short temperature-sensitive period that is a few hours prior to the start of hair morphogenesis. That the temperature during hair morphogenesis is irrelevant for the phenotype of in is consistent with the hypothesis that the only role that in has in wing hair development is to regulate the initiation of hair morphogenesis.


Genetics ◽  
1986 ◽  
Vol 112 (2) ◽  
pp. 217-228
Author(s):  
Mary E Stevens ◽  
Peter J Bryant

ABSTRACT Mutations at the apterous (ap) locus in Drosophila melanogaster produce a variety of developmental defects, including several classes of wing abnormalities. We describe the wing phenotype produced by homozygotes and hemizygotes of three different temperature-sensitive apterous alleles grown at 16, 18, 20, 22, 25, and 29°. We also describe the phenotype produced by each of these three alleles when heteroallelic with the non-temperature-sensitive apc allele. Constant-temperature and temperature-shift experiments show that each of the heteroallelic genotypes can produce several of the previously described apterous phenotypes and that the length of the temperature-sensitive period for a given phenotype depends on the allelic combinations used to measure it. We suggest that the stage-specific requirements of the tissue for gene product, rather than the time of gene expression per se, determine the temperature-sensitive periods for apterous and other loci. The results support the hypothesis that the various wing phenotypes produced by apterous mutations are due to quantitative reductions in the activity of gene product and that failure to meet specific threshold requirements for gene product can lead to qualitatively different phenotypes.


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