scholarly journals TEMPERATURE-SENSITIVE MUTATIONS IN DROSOPHILA MELANOGASTER. XVII. HEAT- AND COLD-SENSITIVE LETHALS ON CHROMOSOME 3

Genetics ◽  
1973 ◽  
Vol 74 (3) ◽  
pp. 509-520
Author(s):  
S Elaine Tasaka ◽  
David T Suzuki

ABSTRACT Ethyl methanesulfonate-treated third chromosome of Drosophila melanogaster were tested for the presence of dominant and recessive temperature-sensitive lethal mutations at 17°, 22° and 29°C. Out of 1,176 chromosomes tested, no dominant ts lethals, 21 heat-sensitive, 22 cold-sensitive and 10 heat-cold-sensitive lethals were recovered. Heat-cold sensitivity was produced by a single mutation in all cases. Sixty-two percent of the ts lethals were fertile as homozygotes in both sexes. Surprisingly, 88% of the ts lethals mapped between st and Sb, a region straddling the centromere and estimated to comprise 12.9% of the genetic length and 55% of the physical length of chromosome 3. All but one of the heat- and cold-sensitive lethals complemented with each other at their respective restrictive temperatures.

Genetics ◽  
1972 ◽  
Vol 70 (1) ◽  
pp. 75-86
Author(s):  
Raja Rosenbluth ◽  
Dean Ezell ◽  
David T Suzuki

ABSTRACT Ethyl methanesulfonate-treated autosomes were screened for the presence of dominant cold-sensitive (DCS) lethal mutations in Drosophila melanogaster. None was found among 6,552 treated and 168 untreated third chromosomes. Twenty-three DCS-L chromosomes which caused death at 17°C but survived at 22°C and 29°C were recovered from 5,046 mutagenized chromosome 2's.—The DCS-L mutations all mapped around dp and appeared to be functionally allelic. Lethality of heterozygotes for most of the DCS-L's occurred over a prolonged interval from the embryonic through the larval instars. Prolonged incubation at 17°C did not demonstrate any maternal effect on zygotic survival.


1973 ◽  
Vol 15 (2) ◽  
pp. 237-254 ◽  
Author(s):  
Helen Mayoh ◽  
David T. Suzuki

Among 3,919 EMS-treated X chromosomes, 25 were retained as cold-sensitive (cs) lethals. That is, more than 20% of flies carrying a cs lethal survive at 22 °C and none at 17 °C and for cs semi-lethals, >30% at 22 °C and <13% at 17 °C. The cs mutations are not randomly distributed, seven being located at the X tip and three being alleles to the right of car. Over half exhibited female sterility or reduced fertility and seven exhibited visible phenotypes characteristic of bobbed and Minute mutations. The possible enrichment for ribosomal protein defects by screening for cold-sensitivity is discussed.


Genetics ◽  
1991 ◽  
Vol 129 (2) ◽  
pp. 409-422 ◽  
Author(s):  
R S Rasooly ◽  
C M New ◽  
P Zhang ◽  
R S Hawley ◽  
B S Baker

Abstract The l(1)TW-6cs mutation is a cold-sensitive recessive lethal mutation in Drosophila melanogaster, that affects both meiotic and mitotic chromosome segregation. We report the isolation of three revertants of this mutation. All three revert both the meiotic and mitotic effects as well as the cold sensitivity, demonstrating that all three phenotypes are due to a single lesion. We further show that these revertants fail to complement an amorphic allele of the nod (no distributive disjunction) locus, which encodes a kinesin-like protein. These experiments demonstrate that l(1)TW-6cs is an antimorphic allele of nod, and we rename it nodDTW. Sequencing of the nod locus on a nodDTW-bearing chromosome reveals a single base change in the putative ATP-binding region of the motor domain of nod. Recessive, loss-of-function mutations at the nod locus specifically disrupt the segregation of nonexchange chromosomes in female meiosis. We demonstrate that, at 23.5 degrees, the meiotic defects in nodDTW/+ females are similar to those observed in nod/nod females; that is, the segregation of nonexchange chromosomes is abnormal. However, in nodDTW/nodDTW females, or in nodDTW/+ females at 18 degrees, we observe a more severe meiotic defect that apparently affects the segregation of both exchange and nonexchange chromosomes. In addition, nodDTW homozygotes and hemizygous males have previously been shown to exhibit mitotic defects including somatic chromosome breakage and loss. We propose that the defective protein encoded by the nodDTW allele interferes with proper chromosome movement during both meiosis and mitosis, perhaps by binding irreversibly to microtubules.


Genetics ◽  
1999 ◽  
Vol 153 (3) ◽  
pp. 1105-1115
Author(s):  
Dong-Ho Kim ◽  
Gretchen Edwalds-Gilbert ◽  
Chengzhen Ren ◽  
Ren-Jang Lin

Abstract The PRP2 gene in Saccharomyces cerevisiae encodes an RNA-dependent ATPase that activates spliceosomes for the first transesterification reaction in pre-mRNA splicing. We have identified a mutation in the elongation methionine tRNA gene EMT1 as a dominant, allele-specific suppressor of the temperature-sensitive prp2-1 mutation. The EMT1-201 mutant suppressed prp2-1 by relieving the splicing block at high temperature. Furthermore, EMT1-201 single mutant cells displayed pre-mRNA splicing and cold-sensitive growth defects at 18°. The mutation in EMT1-201 is located in the anticodon, changing CAT to CAG, which presumably allowed EMT1-201 suppressor tRNA to recognize CUG leucine codons instead of AUG methionine codons. Interestingly, the prp2-1 allele contains a point mutation that changes glycine to aspartate, indicating that EMT1-201 does not act by classical missense suppression. Extra copies of the tRNALeu(UAG) gene rescued the cold sensitivity and in vitro splicing defect of EMT1-201. This study provides the first example in which a mutation in a tRNA gene confers a pre-mRNA processing (prp) phenotype.


Genetics ◽  
1981 ◽  
Vol 98 (4) ◽  
pp. 775-789
Author(s):  
J Gausz ◽  
H Gyurkovics ◽  
G Bencze ◽  
A A M Awad ◽  
J J Holden ◽  
...  

ABSTRACT The region between 86F1,2 and 87B15 on chromosome 3 of Drosophila melanogaster, which contains about 27 polytene chromosome bands including the 87A7 heat-shock locus, has been screened for EMS-induced visible and lethal mutations. We have recovered 268 lethal mutations that fall into 25 complementation groups. Cytogenetic localization of the complementation groups by deficiency mapping is consistent with the notion that each band encodes a single genetic function. We have also screened for mutations at the 87A7 heat shock locus, using a chromosome that has only one copy of the gene encoding the 70,000 dalton heat-shock protein (hsp70). No lethal or visible mutations at 87A7 were identified from 10,719 mutagenized chromosomes, and no female-sterile mutations at 87A7 were recovered from the 1,520 chromosomes whose progeny were tested for female fertility. We found no evidence that a functional hsp70 gene is required for development under laboratory conditions.


Genetics ◽  
1982 ◽  
Vol 100 (4) ◽  
pp. 547-563 ◽  
Author(s):  
Don Moir ◽  
Sue E Stewart ◽  
Barbara C Osmond ◽  
David Botstein

ABSTRACT We isolated 18 independent recessive cold-sensitive cell-division-cycle (cdc) mutants of Saccharomyces cerevisiae, in nine complementation groups. Terminal phenotypes exhibited include medial nuclear division, cytokinesis, and a previously undescribed terminal phenotype consisting of cells with a single small bud and an undivided nucleus. Four of the cold-sensitive mutants proved to be alleles of CDC11, while the remaining mutants defined at least six new cell-division-cycle genes: CDC44, CDC45, CDC48, CDC49, CDC50 and CDC51.—Spontaneous revertants from cold-sensitivity of four of the medial nuclear division cs cdc mutants were screened for simultaneous acquisition of a temperature-sensitive phenotype. The temperature-sensitive revertants of four different cs cdc mutants carried single new mutations, called Sup/Ts to denote their dual phenotype: suppression of the cold-sensitivity and concomitant conditional lethality at 37°. Many of the Sup/Ts mutations exhibited a cell-division-cycle terminal phenotype at the high temperature, and they defined two new cdc genes (CDC46 and CDC47). Two cold-sensitive medial nuclear division cdc mutants representing two different cdc genes were suppressed by different Sup/Ts alleles of another gene which also bears a medial nuclear division function (CDC46). In addition, the cold-sensitive medial nuclear division cdc mutant csH80 was suppressed by a Sup/Ts mutation yielding an unbudded terminal phenotype with an undivided nucleus at the high temperature. This mutation was an allele of CDC32. These results suggest a pattern of interaction among cdc gene products and indicate that cdc gene proteins might act in the cell cycle as complex specific functional assemblies.


2009 ◽  
Vol 45 (2) ◽  
pp. 171-176
Author(s):  
N. P. Matiytsiv ◽  
I. B. Magorivska ◽  
O. V. Shcherbakova ◽  
Ya. I. Chernik ◽  
D. V. Maksymiv

Genetics ◽  
1996 ◽  
Vol 143 (1) ◽  
pp. 67-80 ◽  
Author(s):  
Suzanne M Noble ◽  
Christine Guthrie

Abstract Genetic approaches in Saccharomyces cerevisiae have identified 38 genes required for efficient RNA splicing. The majority have been found by screening (high) temperature-sensitive (ts) mutants for those defective in splicing, an approach limited by the presence of ts hotspots and by the fact that many essential genes rarely mutate to the ts phenotype. To identify novel genes, we screened a collection of 340 cold-sensitive (cs) mutants for those that exhibited diminished splicing of several pre-mRNAs. We isolated 12 mutants in nine complementation groups. Four of these affected known genes (PRP8, PRP16, PRP22, PRP28), three of which encode RNA helicase homologues. Five genes are novel (BRR1, BRR2, BRR3, BRR4, BRR5; Bad Response to Refrigeration); mutations in these genes inhibited splicing before the first chemical step of the reaction. Analysis of BRR2 revealed it to encode an essential member of a new class of RNA helicase-like proteins that includes the yeast antiviral protein Ski2. These data validate the use of cs mutants in genetic screens and raise the possibility that RNA helicase family members are particularly prone to mutation to cold sensitivity.


Genetics ◽  
1986 ◽  
Vol 112 (4) ◽  
pp. 785-802
Author(s):  
Madeline A Crosby ◽  
Elliot M Meyerowitz

ABSTRACT We have conducted a genetic analysis of the region flanking the 68C glue gene cluster in Drosophila melanogaster by isolating lethal and semilethal mutations uncovered by deficiencies which span this region. Three different mutagens were used: ethyl methanesulfonate (EMS), ethyl nitrosourea (ENU) and diepoxybutane (DEB). In the region from 68A3 to 68C11, 64 lethal, semilethal, and visible mutations were recovered. These include alleles of 13 new lethal complementation groups, as well as new alleles of rotated, low xanthine dehydrogenase, lethal(3)517 and lethal(3)B76. Six new visible mutations from within this region were recovered on the basis of their reduced viability; all proved to be semiviable alleles of lethal complementation groups. No significant differences were observed in the distributions of lethals recovered using the three different mutagens. Each lethal was mapped on the basis of complementation with overlapping deficiencies; mutations that mapped within the same interval were tested for complementation, and the relative order of the lethal groups within each interval was determined by recombination. The cytological distribution of genes within the 68A3-68C11 region is not uniform: the region from 68A2,3 to 68B1,3 (seven to ten polytene chromosome bands) contains at least 13 lethal complementation groups and the mutation low xanthine dehydrogenase; the adjoining region from 68B1,3 to 68C5,6 (six to nine bands) includes the 68C glue gene cluster, but no known lethal or visible complementation groups; and the interval from 68C5,6 to 68C10,11 (three to five bands) contains at least three lethal complementation groups and the visible mutation rotated. The developmental stage at which lethality is observed was determined for a representative allele from each lethal complementation group.


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