STUDIES ON THE DEVELOPMENTAL CHARACTERISTICS OF FUSED MUTANTS OF DROSOPHILA MELANOGASTER

1979 ◽  
Vol 21 (3) ◽  
pp. 335-346 ◽  
Author(s):  
Glen G. Wurst ◽  
William P. Hanratty

The development of the lethal and visible effects of 16 independently arising fused mutations was studied. No complementation was observed in any of the 120 heteroallelic combinations of fused mutations. Temperature shift experiments indicated that there is coordinance of expression of all the pleiotropic fused effects, with regard to both temperature sensitive period and degree of expressivity. These studies showed that the expressivity of both the lethal and visible fused effects are directly related to pupal developmental time spent at the restrictive temperature. Gynandromorph studies indicated that all visible effects of the fused mutation develop autonomously and that the thoracic effects are localized in the posterior part of the anterior developmental compartment of the wing disc. These data support the conclusion that the fused locus contains a single functional unit. The data also suggest that the fused gene is expressed simultaneously in each affected tissue of the fly and that the fused product may perform a similar function in each affected part of the fly.

1984 ◽  
Vol 43 (3) ◽  
pp. 257-275 ◽  
Author(s):  
Donald A. R. Sinclair ◽  
Thomas A. Grigliatti ◽  
Thomas C. Kaufman

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.


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.


Development ◽  
1983 ◽  
Vol 76 (1) ◽  
pp. 251-264
Author(s):  
Ernesto Sánchez-Herrero ◽  
Ginés Morata

The mutations at the bithorax locus produce a transformation of anterior haltere into anterior wing. The bx1 allele presents unusual features when compared with other bx alleles. The phenotype of bx1 homozygotes is temperature sensitive but only with regard to the distal and not to the proximal transformation, thus suggesting two different components in the bithorax transformation. The phenotype of bx1 homozygotes is stronger than that of bx1 over the deletion of the gene, suggesting a trans interaction of the bx1 chromosomes which results in mutual partial inactivation. We show by temperature shift and clonal analysis experiments that the decision on whether to differentiate haltere or wing structures is taken at the end of the proliferation period of the mutant disc.


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.


Genetics ◽  
1978 ◽  
Vol 90 (1) ◽  
pp. 49-68
Author(s):  
Yona Kassir ◽  
Giora Simchen

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.


1980 ◽  
Vol 43 (1) ◽  
pp. 75-91
Author(s):  
J. Frankel ◽  
J. Mohler ◽  
A.K. Frankel

Although temperatures of 37.5 and 39 degrees C allow continuous and rapid exponential growth of wild type Tetrahymena thermophila, sudden shifts up to these temperatures can bring about long excess-delays of cell division with accompanying resorption of developing oral primordia. A characteristic parameter of this delay-phenomenon is the physiological transition point, before which delays are maximal and after which they are negligible. When measured at a restrictive temperature that does not induce excess delays (36 degrees C), the end of the temperature-sensitive period of the cell division arrest of mutant cdaA1 precedes the physiological transition point, that of cdaH1 roughly coincides with it, while the entire temperature-sensitive period of cdaC2 comes after the physiological transition point. When cdaA1 cells are exposed to 37.5 degrees C or above, the manifestations of temperature sensitivity are drastically affected: the estimate of the end of the temperature-sensitive period (the execution point) becomes spuriously late, and the characteristic division arrest following heat shocks is not manifested. The differential effects of the higher restrictive temperatures on cdaH1 are most subtle, whereas those on cdaC2 are negligible. We conclude that the excess-delay phenomenon involves a set-back of genemediated processes occurring at specific stages of the cell cycle.


Genetics ◽  
1973 ◽  
Vol 74 (2) ◽  
pp. 267-286
Author(s):  
Leland H Hartwell ◽  
Robert K Mortimer ◽  
Joseph Culotti ◽  
Marilyn Culotti

ABSTRACT One hundred and forty-eight temperature-sensitive cell division cycle (cdc) mutants of Saccharomyces cerevisiae have been isolated and characterized. Complementation studies ordered these recessive mutations into 32 groups and tetrad analysis revealed that each of these groups defines a single nuclear gene. Fourteen of these genes have been located on the yeast genetic map. Functionally related cistrons are not tightly clustered. Mutations in different cistrons frequently produce different cellular and nuclear morphologies in the mutant cells following incubation at the restrictive temperature, but all the mutations in the same cistron produce essentially the same morphology. The products of these genes appear, therefore, each to function individually in a discrete step of the cell cycle and they define collectively a large number of different steps. The mutants were examined by time-lapse photomicroscopy to determine the number of cell cycles completed at the restrictive temperature before arrest. For most mutants, cells early in the cell cycle at the time of the temperature shift (before the execution point) arrest in the first cell cycle while those later in the cycle (after the execution point) arrest in the second cell cycle. Execution points for allelic mutations that exhibit first or second cycle arrest are rather similar and appear to be cistron-specific. Other mutants traverse several cycles before arrest, and its suggested that the latter type of response may reveal gene products that are temperature-sensitive for synthesis, whereas the former may be temperature-sensitive for function. The gene products that are defined by the cdc cistrons are essential for the completion of the cell cycle in haploids of a and α mating type and in a/α diploid cells. The same genes, therefore, control the cell cycle in each of these stages of the life cycle.


1980 ◽  
Vol 43 (1) ◽  
pp. 59-74 ◽  
Author(s):  
J. Frankel ◽  
J. Mohler ◽  
A.K. Frankel

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.


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.


1987 ◽  
Vol 87 (2) ◽  
pp. 305-314 ◽  
Author(s):  
R.M. Hecht ◽  
M. Berg-Zabelshansky ◽  
P.N. Rao ◽  
F.M. Davis

A monoclonal antibody, specific to phosphoproteins in mitotic HeLa cells was found to crossreact with a similar set of proteins in embryos of the nematode, Caenorhabditis elegans. In C. elegans, as in mammalian cells, the highly conserved antigenic epitope is associated with a family of high molecular weight polypeptides. The antigenic reactivity of these multiple proteins also depends on their phosphorylation, since antibody binding is reduced after alkaline phosphatase treatment. The antigens are detected at the centrosomes, and in the nuclear region and surrounding cytoplasm of mitotic cells. The significance of these antigens is emphasized by their absence at restrictive temperature in embryos of the temperature-sensitive embryonic-arrest mutant, emb-29V. Furthermore, temperature shift-down experiments suggest that the emb-29 mutation defines a cell division cycle function that affects an essential activity required for progression into M phase.


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