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.

Temperature-sensitive mutations affecting cortical morphogenesis and cell division in Paramecium tetraurelia

1982 ◽  
Vol 60 (10) ◽  
pp. 2296-2308 ◽  
Author(s):  
Donald Jones ◽  
James D. Berger
Keyword(s):  
Cell Division ◽  
Cell Surface ◽  
Posterior Part ◽  
Gene Mutations ◽  
Temperature Sensitive ◽  
Basal Bodies ◽  
Paramecium Tetraurelia ◽  
Fission Process ◽  
Daughter Cells ◽  
Recessive Genes

Nine temperature-sensitive gene mutations affecting cellular morphogenesis were analysed and shown to be single recessive genes. Their phenotypes fall into three classes: small mutants (sm) which interfere with cell surface and basal body proliferation to produce short cells; defective fission zone mutants (dfz) which do not form a complete fission zone during cell division; and defective constriction mutants (dc) which form a normal fission zone, but do not constrict properly. In sm2 cells there is a reduction in the number of basal bodies and in the amount of cell surface produced preceding fission. This results in the production of truncated daughter cells in which most of the normal structures of either the anterior or posterior part of the cell are highly reduced or missing. Production of basal bodies in gullet primordia is also abnormal. The dfz mutants act early in the fission process to block the formation of the fission zone which precedes the formation of the fission furrow. The dc mutations act later in the fission process and lead to failure of daughter cell separation. One mutant, dc3, also shows slightly reduced proliferation of cell surface. This defect occurs prior to fission.

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 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.

Patterning of dopaminergic neurotransmitter identity among Caenorhabditis elegans ray sensory neurons by a TGFbeta family signaling pathway and a Hox gene

Development ◽  
1999 ◽  
Vol 126 (24) ◽  
pp. 5819-5831 ◽  
Author(s):  
R. Lints ◽  
S.W. Emmons
Keyword(s):  
Caenorhabditis Elegans ◽  
Heat Shock ◽  
Signaling Pathway ◽  
Cell Fate ◽  
Sensory Neurons ◽  
Ectopic Expression ◽  
Temperature Shift ◽  
Temperature Sensitive ◽  
Loss Of Function ◽  
Hox Gene

We have investigated the mechanism that patterns dopamine expression among Caenorhabditis elegans male ray sensory neurons. Dopamine is expressed by the A-type sensory neurons in three out of the nine pairs of rays. We used expression of a tyrosine hydroxylase reporter transgene as well as direct assays for dopamine to study the genetic requirements for adoption of the dopaminergic cell fate. In loss-of-function mutants affecting a TGFbeta family signaling pathway, the DBL-1 pathway, dopaminergic identity is adopted irregularly by a wider subset of the rays. Ectopic expression of the pathway ligand, DBL-1, from a heat-shock-driven transgene results in adoption of dopaminergic identity by rays 3–9; rays 1 and 2 are refractory. The rays are therefore prepatterned with respect to their competence to be induced by a DBL-1 pathway signal. Temperature-shift experiments with a temperature-sensitive type II receptor mutant, as well as heat-shock induction experiments, show that the DBL-1 pathway acts during an interval that extends from two to one cell generation before ray neurons are born and begin to differentiate. In a mutant of the AbdominalB class Hox gene egl-5, rays that normally express EGL-5 do not adopt dopaminergic fate and cannot be induced to express DA when DBL-1 is provided by a heat-shock-driven dbl-1 transgene. Therefore, egl-5 is required for making a subset of rays capable of adopting dopaminergic identity, while the function of the DBL-1 pathway signal is to pattern the realization of this capability.

The conditional medaka mutation eyeless uncouples patterning and morphogenesis of the eye

Development ◽  
2000 ◽  
Vol 127 (9) ◽  
pp. 1911-1919 ◽  
Author(s):  
S. Winkler ◽  
F. Loosli ◽  
T. Henrich ◽  
Y. Wakamatsu ◽  
J. Wittbrodt
Keyword(s):  
Cell Transplantation ◽  
Retinal Development ◽  
Marker Gene ◽  
Temperature Shift ◽  
Lateral Wall ◽  
Temperature Sensitive ◽  
Optic Vesicle ◽  
Optic Vesicles ◽  
Development Temperature ◽  
Vertebrate Eye

In early vertebrate eye development, the retinal anlage is specified in the anterior neuroectoderm. During neurulation, the optic vesicles evaginate from the lateral wall of the prosencephalon. Here we describe the temperature-sensitive mutation eyeless in the Japanese medakafish. Marker gene analysis indicates that, whereas, specification of two retinal primordia and proximodistal patterning takes place in the mutant embryo, optic vesicle evagination does not occur and subsequent differentiation of the retinal primordia is not observed. The mutation eyeless thus uncouples patterning and morphogenesis at early steps of retinal development. Temperature-shift experiments indicate a requirement for eyeless activity prior to optic vesicle evagination. Cell transplantation shows that eyeless acts cell autonomously.

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.

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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