Temperature-sensitive mutations affecting the regenerative sodium channel in Drosophila melanogaster

Nature ◽  
1974 ◽  
Vol 248 (5444) ◽  
pp. 166-168 ◽  
Author(s):  
LEONARD E. KELLY
Genetics ◽  
1995 ◽  
Vol 139 (4) ◽  
pp. 1679-1688 ◽  
Author(s):  
G Feng ◽  
P Deák ◽  
D P Kasbekar ◽  
D W Gil ◽  
L M Hall

Abstract Voltage-sensitive sodium channels play a key role in nerve cells where they are responsible for the increase in sodium permeability during the rising phase of action potentials. In Drosophila melanogaster a subset of temperature-sensitive paralytic mutations affect sodium channel function. One such mutation is temperature-induced paralysis locus E (tipE), which has been shown by electrophysiology and ligand binding studies to reduce sodium channel numbers. Three new gamma-ray-induced tipE alleles associated with either visible deletions in 64AB or a translocation breakpoint within 64B2 provide landmarks for positional cloning of tipE. Beginning with the flanking cloned gene Ras2, a 140-kb walk across the translocation breakpoint was completed. Germline transformation using a 42-kb cosmid clone and successively smaller subclones localized the tipE gene within a 7.4-kb genomic DNA segment. Although this chromosome region is rich in transcripts, only three overlapping mRNAs (5.4, 4.4, and 1.7 kb) lie completely within the smallest rescuing construct. The small sizes of the rescuing construct and transcripts suggest that tipE does not encode a standard sodium channel alpha-subunit with four homologous repeats. Sequencing these transcripts will elucidate the role of the tipE gene product in sodium channel functional regulation.


1974 ◽  
Vol 16 (4) ◽  
pp. 713-735 ◽  
Author(s):  
David T. Suzuki

In screening Drosophila melanogaster for mutations which cause paralysis at 29cC and recovery of mobility at 22cC, 11 temperature-sensitive (ts) mutants were detected among 1.35 × 106 flies screened. These mutations fell into 3 loci, paralytic (parats), shibire (shits) and stoned (stnts). All three loci affect neurological development. The best explanation for parats appears to be an effect on the inhibitory neuronal system. The shi alleles affect an array of developmental events from early embryos to adults. The pattern of heat-induced changes in shits1 electroretinograms (ERG) is consistent with a ts membranal defect. This is supported by a ts resistance of shits flies to tetrodotoxin which specifically blocks the sodium channel of nerves.The final locus, stn, causes sensitivity to the trauma of temperature changes. A jump response observed when a light is turned off is related to a large "offtransient" in ERGs which is correlated with a simultaneous muscle spike. The property of temperature-sensitivity allows greater analytic powers in the study of neurological mutants.


Genetics ◽  
1973 ◽  
Vol 74 (4) ◽  
pp. 619-631
Author(s):  
D L Hartl

ABSTRACT The recovery of the SD chromosome from a heterozygous SD male increases with brood. This is independent of the age of the female, occurs during the time the sperm are stored in the females, disappears when the segregation distortion is suppressed, and is temperature-sensitive-temperature shocks above or below 25°C applied to the mature sperm both tend to accelerate the increase in the recovery of SD. All this suggests the existence of a class of sperm affected by SD in which the sperm are able to fertilize eggs for a short time following ejaculation but become dysfunctional thereafter.


Development ◽  
1978 ◽  
Vol 47 (1) ◽  
pp. 111-120
Author(s):  
M. Bownes ◽  
B. D. Hames

A number of female sterile mutations on the first and third chromosomes of Drosophila melanogaster have been screened for defects in the yolk proteins using polyacrylamide gel electrophoresis. Two new mutants were identified. 6m45 accumulates all three yolk proteins (YP1, YP2 and YP3) in the haemolymph but they are all absent from the ovaries suggesting it is a yolk-protein-uptake mutant. In contrast, 1163 is a temperature-sensitive mutation with a large reduction in the quantity of YP1 in the haemolymph and ovaries at 29 °C. Both mutants are autonomous in ovary transplant experiments.


Development ◽  
1980 ◽  
Vol 55 (1) ◽  
pp. 247-256
Author(s):  
Thomas G. Wilson

A new allele of the suppressor of forked [su(f)] mutation in Drosophila melanogaster has been found and designated 1(1)su(f)ts76a. It is temperature-sensitive for suppression of forked (f) and has additional temperature-sensitive phenotypes of lethality, female sterility, and abnormal bristle formation at 29 °C. It closely resembles two other conditional alleles of su(f), 1(1)su(f)ts67g and 1(1)ts726. Female sterility at 29 °C is characterized by both disorganized egg chambers in the ovarioles and also chorion-deficient oocytes. Both of these abnormalities may be the result of premature follicle cell death. The observations on 1(1)su(f)ts76a are consistent with the proposal that the similar allele, 1(1)ts726, is a cell-lethal mutation specifically affecting mitotically active cells.


Heredity ◽  
2009 ◽  
Vol 104 (2) ◽  
pp. 125-134 ◽  
Author(s):  
K S Pedersen ◽  
M C Codrea ◽  
C J Vermeulen ◽  
V Loeschcke ◽  
E Bendixen

2009 ◽  
Vol 284 (35) ◽  
pp. 23558-23563 ◽  
Author(s):  
Lior Cohen ◽  
Yehu Moran ◽  
Amir Sharon ◽  
Daniel Segal ◽  
Dalia Gordon ◽  
...  

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