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.

scholarly journals Identification and Characterization of Genes That Interact With lin-12 in Caenorhabditis elegans

Genetics ◽  
1997 ◽  
Vol 147 (4) ◽  
pp. 1675-1695 ◽  
Author(s):  
Frans E Tax ◽  
James H Thomas ◽  
Edwin L Ferguson ◽  
H Robert Horvitzt
Keyword(s):  
Cell Fate ◽  
Low Frequency ◽  
Signal Transduction Pathway ◽  
Temperature Shift ◽  
Egg Laying ◽  
Null Alleles ◽  
Temperature Sensitive ◽  
Loss Of Function ◽  
Gain Of Function ◽  
Suppressor Mutations

Abstract We identified and characterized 14 extragenic mutations that suppressed the dominant egg-laying defect of certain lin-12 gain-of-function mutations. These suppressors defined seven genes: sup-l7, lag-2, sel-4, sel-5, sel-6, sel-7 and sel-8. Mutations in six of the genes are recessive suppressors, whereas the two mutations that define the seventh gene, lag-2, are semi-dominant suppressors. These suppressor mutations were able to suppress other lin-12 gain-of-function mutations. The suppressor mutations arose at a very low frequency per gene, 10-50 times below the typical loss-of-function mutation frequency. The suppressor mutations in sup1 7 and lag-2 were shown to be rare non-null alleles, and we present evidence that null mutations in these two genes cause lethality. Temperature-shift studies for two suppressor genes, sup1 7and lag-2, suggest that both genes act at approximately the same time as lin-12in specifying a cell fate. Suppressor alleles of six of these genes enhanced a temperature-sensitive loss-of-function allele of glp-1, a gene related to lin-12 in structure and function. Our analysis of these suppressors suggests that the majority of these genes are part of a shared lin-12/glp-1 signal transduction pathway, or act to regulate the expression or stability of lin-12 and glp-1.

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.

The cold-sensitive period for frizzled in the development of wing hair polarity ends prior to the start of hair morphogenesis

1994 ◽  
Vol 46 (2) ◽  
pp. 101-107 ◽  
Author(s):  
Paul N. Adler ◽  
Jeannette Charlton ◽  
Katherine H. Jones ◽  
Jingchun Liu
Keyword(s):  
Sensitive Period ◽  
Wing Hair ◽  
Cold Sensitive ◽  
Hair Morphogenesis

scholarly journals Tyrosine kinase oncogenes abrogate interleukin-3 dependence of murine myeloid cells through signaling pathways involving c-myc: conditional regulation of c-myc transcription by temperature-sensitive v-abl.

1989 ◽  
Vol 9 (12) ◽  
pp. 5685-5695 ◽  
Author(s):  
J L Cleveland ◽  
M Dean ◽  
N Rosenberg ◽  
J Y Wang ◽  
U R Rapp
Keyword(s):  
Protein Synthesis ◽  
Tyrosine Kinase ◽  
Temperature Shift ◽  
Expression Vectors ◽  
Temperature Sensitive ◽  
Permissive Temperature ◽  
Wild Type ◽  
Interleukin 3 ◽  
Temperature Sensitive Mutants ◽  
Growth Properties

Retroviral expression vectors carrying the tyrosine kinase oncogenes abl, fms, src, and trk abrogate the requirements of murine myeloid FDC-P1 cells for interleukin-3 (IL-3). Factor-independent clones constitutively express c-myc in the absence of IL-3, whereas in parental cultures c-myc transcription requires the presence of the ligand. To directly test the effect of a tyrosine kinase oncogene on c-myc expression, retroviral constructs containing three different temperature-sensitive mutants of v-abl were introduced into myeloid IL-3-dependent FDC-P1 and 32D cells. At the permissive temperature, clones expressing temperature-sensitive abl behaved like wild-type abl-containing cells in their growth properties and expressed c-myc constitutively. Temperature shift experiments demonstrated that both IL-3 abrogation and the regulation of c-myc expression correlated with the presence of functional v-abl. Induction of c-myc expression by reactivation of temperature-sensitive v-abl mimicked c-myc induction by IL-3 in that it did not require protein synthesis and occurred at the level of transcription, with effects on both initiation and a transcription elongation block. However, v-abl-regulated FDC-P1 cell growth differed from IL-3-regulated growth in that c-fos and junB, which are normally induced by IL-3, were not induced by activation of v-abl.

scholarly journals ATP-Dependent Localization of the Herpes Simplex Virus Capsid Protein VP26 to Sites of Procapsid Maturation

2000 ◽  
Vol 74 (3) ◽  
pp. 1468-1476 ◽  
Author(s):  
Jung Hee I. Chi ◽  
Duncan W. Wilson
Keyword(s):  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Fluorescent Protein ◽  
Cold Sensitivity ◽  
Temperature Sensitive ◽  
Permissive Temperature ◽  
Protein Fusion ◽  
Capsid Shell ◽  
Green Fluorescent ◽  
Simplex Virus

ABSTRACT The herpes simplex virus type 1 (HSV-1) capsid shell is composed of four major polypeptides, VP5, VP19c, VP23, and VP26. VP26, a 12-kDa polypeptide, is associated with the tips of the capsid hexons formed by VP5. Mature capsids form upon angularization of the shell of short-lived, fragile spherical precursors termed procapsids. The cold sensitivity and short-lived nature of the procapsid have made its isolation and biochemical analysis difficult, and it remains unclear whether procapsids contain bound VP26 or whether VP26 is recruited following shell angularization. By indirect immunocytochemical analysis of virally expressed VP26 and by direct visualization of a transiently expressed VP26-green fluorescent protein fusion, we show that VP26 fails to specifically localize to intranuclear procapsids accumulated following incubation of the temperature-sensitive HSV mutanttsProt.A under nonpermissive conditions. However, following a downshift to the permissive temperature, which allows procapsid maturation to proceed, VP26 was seen to concentrate at intranuclear sites which also contained epitopes specific to mature, angularized capsids. Like the formation of these epitopes, the association of VP26 with maturing capsids was blocked in a reversible fashion by the depletion of intracellular ATP. We conclude that unlike the other major capsid shell proteins, VP26 is recruited in an ATP-dependent fashion after procapsid maturation begins.

scholarly journals MEIOTIC RECOMBINATION AND DNA SYNTHESIS IN A NEW CELL CYCLE MUTANT OF SACCHAROMYCES CEREVISIAE

Genetics ◽  
1978 ◽  
Vol 90 (1) ◽  
pp. 49-68
Author(s):  
Yona Kassir ◽  
Giora Simchen
Keyword(s):  
Cell Cycle ◽  
Dna Replication ◽  
Dna Synthesis ◽  
Nuclear Division ◽  
Temperature Shift ◽  
Temperature Sensitive ◽  
Restrictive Temperature ◽  
Permissive Temperature ◽  
Essential Function ◽  
Normal Meiosis

ABSTRACT Vegetative cells carrying the new temperature-sensitive mutation cdc40 arrest at the restrictive temperature with a medial nuclear division phenotype. DNA replication is observed under these conditions, but most cells remain sensitive to hydroxyurea and do not complete the ongoing cell cycle if the drug is present during release from the temperature block. It is suggested that the cdc40 lesion affects an essential function in DNA synthesis. Normal meiosis is observed at the permissive temperature in cdc40 homozygotes. At the restrictive temperature, a full round of premeiotic DNA replication is observed, but neither commitment to recombination nor later meiotic events occur. Meiotic cells that are already committed to the recombination process at the permissive temperature do not complete it if transferred to the restrictive temperature before recombination is realized. These temperature shift-up experiments demonstrate that the CDC40 function is required for the completion of recombination events, as well as for the earlier stage of recombination commitment. Temperature shift-down experiments with cdc40 homozygotes suggest that meiotic segregation depends on the final events of recombination rather than on commitment to recombination.

scholarly journals Evidence of a dual function in fl(2)d, a gene needed for Sex-lethal expression in Drosophila melanogaster.

Genetics ◽  
1992 ◽  
Vol 130 (3) ◽  
pp. 597-612 ◽  
Author(s):  
B Granadino ◽  
A San Juán ◽  
P Santamaria ◽  
L Sánchez
Keyword(s):  
Drosophila Melanogaster ◽  
Germ Cells ◽  
Sensitive Period ◽  
Dual Function ◽  
Temperature Sensitive ◽  
Permissive Temperature ◽  
Loss Of Function ◽  
Germline Development ◽  
Suppression Effect ◽  
Pole Cells

Abstract In Drosophila melanogaster, the female sexual development of the soma and the germline requires the activity of the gene Sxl. The somatic cells need the function of the gene fl(2)d to follow the female developmental pathway, due to its involvement in the female-specific splicing of Sxl RNA. Here we report the analysis of both fl(2)d1 and fl(2)d2 mutations: (1) fl(2)d1 is a temperature-sensitive mutation lethal in females and semilethal in males; (2) fl(2)d2 is lethal in both sexes; (3) the fl(2)d1/fl(2)d2 constitution is temperature-sensitive and lethal in females, while semilethal in males. The temperature-sensitive period of fl(2)d1 in females expands the whole development. SxlM1 partially suppresses the lethality of fl(2)d1 homozygous females and that of fl(2)d1/fl(2)d2 constitution, whereas it does not suppress the lethality of fl(2)d2 homozygous females. The addition of extra Sxl+ copies does not increase the suppression effect of SxlM1. The fl(2)d1 mutation in homozygosis and the fl(2)d1/fl(2)d2 constitution, but not the fl(2)d2 in homozygosis, partially suppress the lethality of SxlM1 males. This suppression is not prevented by the addition of extra Sxl+ copies. The semilethality of both fl(2)d1 and fl(2)d1/fl(2)d2 males, and the lethality of fl(2)d2 males, is independent of Sxl function. There is no female synergistic lethality between mutations at fl(2)d and neither at sc or da. However, the female synergistic lethality between mutations at Sxl and either sc or da is increased by fl(2)d mutations. We have analyzed the effect of the fl(2)d mutations on the germline development of both females and males. For that purpose, we carried out the clonal analysis of fl(2)d1 in the germline. In addition, pole cells homozygous for fl(2)d2 were transplanted into wild-type host embryos, and we checked whether the mutant pole cells were capable of forming functional gametes. The results indicated that fl(2)d mutant germ cells cannot give rise to functional oocytes, while they can form functional sperm. Moreover, SxlM1 suppresses the sterility of the fl(2)d1 homozygous females developing at the permissive temperature. Thus, with respect to the development of the germline the fl(2)d mutations mimic the behavior of loss-of-function mutations at the gene Sxl. Females double heterozygous for fl(2)d and snf1621 are fully viable and fertile. fl(2)d2 in heterozygosis partially suppresses the phenotype of female germ cells homozygous for snf1621; however, this is not the case with the fl(2)d1 mutation. The fl(2)d mutations partially suppress the phenotype of the female germ cells homozygous for ovoDIrSI.(ABSTRACT TRUNCATED AT 400 WORDS)

Temperature-sensitive periods of mutations affecting cell division in Tetrahymena thermophila

1980 ◽  
Vol 43 (1) ◽  
pp. 59-74 ◽  
Author(s):  
J. Frankel ◽  
J. Mohler ◽  
A.K. Frankel
Keyword(s):  
Cell Division ◽  
Tetrahymena Thermophila ◽  
Sensitive Period ◽  
Temperature Sensitive ◽  
Restrictive Temperature ◽  
Permissive Temperature ◽  
Physiological Effects ◽  
Sensitive Periods ◽  
Phenotypic Abnormality ◽  
Mutant Cells

Temperature-sensitive periods were determined by application of temperature shifts and shocks to 3 temperature-sensitive cell division arrest (cda) mutants of Tetrahymena thermophila. A restrictive temperature, 36 degrees C, was found at which all 3 mutants are fully penetrant, yet other physiological effects are minimal. At this temperature, the temperature-sensitive period of cdaC2 is a unique 5-min period in mid-division, that of cdaA1 is a similarly brief period situated about 0.5 h prior to cell division, while the temperature-sensitive period of cdaH1 is 20 to 30 min long and immediately precedes cell division. These periods either coincide with (cdaC2, cdaH1) or immediately precede (cdaA1) the onset of phenotypic abnormality at the restrictive temperature. Brief exposure to 36 degrees C during the temperature-sensitive period in any of these mutants brings about irreversible arrest of division furrows in progress or preparation. Mutant cells suffering such arrest can, however, divide again at a permissive temperature by forming new furrows at different sites.

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.

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