scholarly journals GENETIC AND DEVELOPMENTAL ANALYSIS OF A TEMPERATURE-SENSITIVE MINUTE MUTATION OF DROSOPHILA MELANOGASTER

Genetics ◽  
1981 ◽  
Vol 97 (3-4) ◽  
pp. 581-606 ◽  
Author(s):  
Donald A R Sinclair ◽  
David T Suzuki ◽  
Thomas A Grigliatti
Keyword(s):  
Larval Instar ◽  
Temperature Shift ◽  
Heat Pulse ◽  
Sensitive Period ◽  
Temperature Sensitive ◽  
Direct Effects ◽  
First Instar ◽  
Reciprocal Temperature ◽  
Morphological Defects ◽  
Developmental Analysis

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.

scholarly journals Effects of a temperature-sensitiveMinutemutation on gene expression inDrosophila melanogaster

1984 ◽  
Vol 43 (3) ◽  
pp. 257-275 ◽  
Author(s):  
Donald A. R. Sinclair ◽  
Thomas A. Grigliatti ◽  
Thomas C. Kaufman
Keyword(s):  
Gene Expression ◽  
Temperature Shift ◽  
Temperature Sensitive ◽  
Restrictive Temperature ◽  
Gene Products ◽  
The Past ◽  
Reciprocal Temperature ◽  
Sex Comb ◽  
Mutant Phenotypes

SUMMARYMinute(M) lesions exhibit a striking propensity for interacting with many different mutations. In the past, few attempts have been made to explain these diverse phenomena. This study describes a variety of temperature-sensitive (ts) interactions exhibited by the ts third chromosomeMinutemutationM(3)LS4Q-III(Q-III). Most of these interactions (i.e. those involvingvg, cp, Dl, DfdorLy) reflectQ-III-induced enhancement of the respective mutant phenotypes at the restrictive temperature. However,Q-IIIalso suppresses the extra-sex-comb phenotypes ofPcandMscat 29 °C and evokes lethal and bristle traits when combined withJ34eat the restrictive temperature. All of these interactions are characteristic of non-tsMinutelesions and thus they appear to be correlated with general physiological perturbations associated with theMsyndrome. In addition, our findings show that mutations that affect ribosome production and/or function, namelysu(f)ts67gandbbts−1, exhibit interactions comparable to those elicited byQ-III. Hence, in accordance with previous findings, we argue that most of theQ-IIIinteractions can be attributed to reduced translational capacity at the restrictive temperature. Finally, reciprocal temperature shift studies were used to delineate TSPs for interactions betweenQ-IIIandvg(mid to late second instar),cp(about mid-third instar),Dfd(early third instar) andDl(late second to mid third instar). We believe that these TSPs represent developmental intervals during which the respective gene products are utilized.

scholarly journals A Caenorhabditis elegans RNA polymerase II gene, ama-1 IV, and nearby essential genes.

Genetics ◽  
1988 ◽  
Vol 118 (1) ◽  
pp. 61-74
Author(s):  
T M Rogalski ◽  
D L Riddle
Keyword(s):  
Caenorhabditis Elegans ◽  
Rna Polymerase ◽  
Rna Polymerase Ii ◽  
Gamma Ray ◽  
Temperature Shift ◽  
Developmental Rate ◽  
Egg Laying ◽  
Essential Genes ◽  
Sensitive Period ◽  
Temperature Sensitive

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.

scholarly journals ON THE DEVELOPMENT OF ECTOPIC EYES IN DROSOPHILA MELANOGASTER PRODUCED BY THE MUTATION EXTRA EYE (EE)

Genetics ◽  
1985 ◽  
Vol 111 (1) ◽  
pp. 67-88
Author(s):  
William K Baker ◽  
David J Marcey ◽  
M Catharine McElwain
Keyword(s):  
Cell Death ◽  
Larval Instar ◽  
Temperature Shift ◽  
Mirror Image ◽  
Temperature Sensitive ◽  
Cell Counts ◽  
Extensive Cell Death ◽  
Extensive Cell ◽  
Cell Autonomy ◽  
Ectopic Eyes

ABSTRACT The mutation ee often produces an ectopic eye on the vertex that is a mirror image partial duplication of the normal eye on the ipsilateral side of the head. The pattern of the duplication and a clonal analysis by mitotic recombination indicate that the duplications are of dorsal eye and orbital structures. Large ectopic eyes (more than 100 ommatidia) and their surrounding bristles may be produced without cuticular deficiencies. The penetrance of ee is temperature dependent with penetrance higher (72%) at 25° and 29° than at 19° (43%). Temperature shift experiments show two temperature-sensitive periods: one at midembryogenesis, the other at mid-first larval instar. Microscopic examination of ee late-second and third instar imaginal cephalic discs show no indication of growth of the extra tissue needed to produce the duplication until after mid-third instar. This was confirmed by cell counts of ee and wild-type discs. There is no evidence of differential cell death in the two types of discs at this stage, although much earlier cell death is postulated. Tests for cell autonomy of the mutation by the production of morphogenetic clones suggest nonautonomy. Formation of pattern duplications by mutant genes is discussed in terms of cell death that eliminates whole developmental compartments, restricted cell death that occurs within a compartment, extensive cell death within a compartment and proliferative growth unassociated with cell lethality.

Analysis of the temperature-sensitive period of the short-1 mutation affecting stomatogenesis in Paramecium tetraurelia

1987 ◽  
Vol 88 (2) ◽  
pp. 241-250
Author(s):  
LAI-WA TAM ◽  
STEPHEN F. NG
Keyword(s):  
Heat Shock ◽  
Sexual Reproduction ◽  
Temperature Shift ◽  
High Sensitivity ◽  
Sensitive Period ◽  
Temperature Sensitive ◽  
Basal Bodies ◽  
Paramecium Tetraurelia ◽  
Membrane Growth ◽  
Development Temperature

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.

scholarly journals The recovery and preliminary examination of a temperature sensitive suppressor of the cryptocephal mutant of Drosophila melanogaster

1981 ◽  
Vol 38 (3) ◽  
pp. 297-314 ◽  
Author(s):  
John C. Sparrow
Keyword(s):  
Drosophila Melanogaster ◽  
Temperature Shift ◽  
Sensitive Period ◽  
Temperature Sensitive ◽  
Induced Mutations ◽  
Chitin Synthesis ◽  
Preliminary Examination

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.

scholarly journals RECOVERY AND CHARACTERIZATION OF TEMPERATURE-SENSITIVE MUTATIONS AFFECTING ADULT VIABILITY IN DROSOPHILA MELANOGASTER

Genetics ◽  
1986 ◽  
Vol 113 (2) ◽  
pp. 367-389
Author(s):  
Theodore Homyk ◽  
Donald A R Sinclair ◽  
David T L Wong ◽  
Thomas A Grigliatti
Keyword(s):  
Temperature Shift ◽  
The Other ◽  
Temperature Sensitive ◽  
Cell Type ◽  
Lethal Mutations ◽  
Preimaginal Development ◽  
Depth Analysis ◽  
Mosaic Analysis ◽  
Developmental Analysis

ABSTRACT Temperature-sensitive (ts) autonomous cell-lethal mutations have been used extensively to study important developmental phenomena, such as pattern formation, in Drosophila. Their utility would be enhanced considerably if it were possible to establish which cell type is primarily affected by each lesion. To facilitate such an approach we have isolated and characterized 21 EMS- induced X-linked adult-lethal (adl) mutants, 16 of which are ts. Most of these lesions also elicit ts lethal effects during preimaginal development. They represent 19 different loci distributed randomly along the X chromosome. The general properties of these mutations are described. In addition, results of an in-depth analysis (focus mapping and, in some cases, temperature shift and heat-pulse studies) of four strains, adl-1ts  1, sesE, adl-2ts  1 and rex are reported. Two major temperature-sensitive periods (TSPs) of adl-1 lethality were resolved: one during the second half of embryogenesis and the other coinciding with pupariation. Mosaic analysis revealed separate mesodermal foci for leg paralysis. Developmental analysis of adl-1 embryos suggest that the adl-1 product may be required for maintenance of muscle tissue. Two discrete TSPs of sesE lethality exist: one during the second instar and the other extending from late third instar to early pupation. Mosaic analysis of sesE lethality resolved a pair of neural foci, each of which appears to incorporate three separate foci for leg paralysis. Mosaic analysis of adl-2ts  1 revealed the existence of paired lethal foci that appear to map to the vicinity of the subesophageal ganglion. Analysis of rex mosaics resolved separate mesodermal foci for leg paralysis.

TEMPERATURE-DEPENDENT EXPRESSION OF THE APTEROUS PHENOTYPE IN DROSOPHILA MELANOGASTER

Genetics ◽  
1986 ◽  
Vol 112 (2) ◽  
pp. 217-228
Author(s):  
Mary E Stevens ◽  
Peter J Bryant
Keyword(s):  
Gene Expression ◽  
Drosophila Melanogaster ◽  
Gene Product ◽  
Constant Temperature ◽  
Temperature Shift ◽  
Sensitive Period ◽  
Temperature Sensitive ◽  
Temperature Dependent ◽  
Developmental Defects ◽  
Per Se

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.

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

1986 ◽  
Vol 28 (6) ◽  
pp. 982-990 ◽  
Author(s):  
Namboori B. Raju
Keyword(s):  
Neurospora Crassa ◽  
High Temperatures ◽  
Low Temperatures ◽  
Meiotic Prophase ◽  
Temperature Shift ◽  
Sensitive Period ◽  
Temperature Sensitive ◽  
Limited Temperature ◽  
Increasing Temperature ◽  
Two Temperature

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.

scholarly journals SEX CHROMOSOME MEIOTIC DRIVE SYSTEMS IN DROSOPHILA MELANOGASTER I. ABNORMAL SPERMATID DEVELOPMENT IN MALES WITH A HETEROCHROMATIN-DEFICIENT X CHROMOSOME (sc  4  sc  8)

Genetics ◽  
1975 ◽  
Vol 79 (4) ◽  
pp. 613-634
Author(s):  
W J Peacock ◽  
George L Gabor Miklos ◽  
D J Goodchild
Keyword(s):  
Electron Microscopy ◽  
Drosophila Melanogaster ◽  
Sex Chromosome ◽  
Light And Electron Microscopy ◽  
Temperature Shift ◽  
Meiotic Drive ◽  
Sensitive Period ◽  
Temperature Sensitive ◽  
Electron Microscopes ◽  
Drive Systems

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.

scholarly journals The Drosophila tissue polarity gene inturned functions prior to wing hair morphogenesis in the regulation of hair polarity and number.

Genetics ◽  
1994 ◽  
Vol 137 (3) ◽  
pp. 829-836 ◽  
Author(s):  
P N Adler ◽  
J Charlton ◽  
W J Park
Keyword(s):  
Temperature Shift ◽  
Null Alleles ◽  
Cold Sensitivity ◽  
Sensitive Period ◽  
Temperature Sensitive ◽  
Heat Sensitivity ◽  
Permissive Temperature ◽  
Wing Hair ◽  
Almost All ◽  
Hair Morphogenesis

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.

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