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Biomedical subjects

B Ganetzky

Publications and source records attributed to B Ganetzky.

83 records · Page 5Linked to original sources
PubMed1986

Neurogenetic analysis of Drosophila mutations affecting sodium channels: synergistic effects on viability and nerve conduction in double mutants involving tip-E.

In previous work it was shown that parats (paralyzed, temperature-sensitive, 1-53.9) and napts (no action potential, temperature-sensitive, 2-56.2), two temperature-sensitive paralytic mutations that block nerve conduction at restrictive temperatures, interact synergistically in double mutants causing unconditional lethality. This interaction is now shown to include tip-E (temperature-induced paralysis, 3-13.5), another temperature-sensitive paralytic mutation. There is an allele-dependent interaction between tip-E and various para alleles resulting in the unconditional lethality of the most extreme double mutant combinations. The pattern of this allele-dependency is strikingly different from that previously reported for napts and para in that the para alleles that interact strongest with napts interact weakest with tip-E and vice-versa. Double mutants of tip-E with napts also display greatly reduced viability. Surviving double mutants of tip-E with either parats1 or napts are weak and exhibit enhanced temperature sensitivity for both paralysis and nerve conduction failure. In addition, in a tip-E background, mutant para alleles enhance temperature-sensitive paralysis even when heterozygous with para+. The results of these studies suggest that tip-E shares related function with para and nap. It is proposed that tip-E, like para and nap exerts an effect at some level on the structure, function, or stability of sodium channels.

Alleles↗
PubMed1984

On the components of segregation distortion in Drosophila melanogaster. III. Nature of enhancer of SD.

Analysis of X-ray-induced deletions in the Segregation Distorter (SD) chromosome, SD-5, revealed that this chromosome had a gene proximal to lt in the centric heterochromatin of 2L that strongly enhanced the meiotic drive caused by the SD chromosome. This Enhancer of Segregation Distortion [E(SD)] locus had not been characterized in earlier studies of SD chromosomes because it cannot be readily separated by recombination from the Responder (Rsp) locus in the proximal heterochromatin of 2R.--To determine whether E(SD) is a general component of all SD chromosomes and to examine further its effects on distortion, we produced deletions of E(SD) in three additional SD chromosomes. Analysis of these deletions leads to the following conclusions: (1) along with Sd and Rsp, E(SD) is common to all SD chromosomes; (2) the E(SD) allele on each SD chromosome enhances distortion by the same amount, which indicates that allelic variation at the E(SD) locus is not responsible for the different drive strengths seen among SD chromosomes; (3) E(SD) causes very little or no distortion by itself in the absence of Sd; (4) E(SD), like Sd, acts in a dosage-dependent manner; (5) E(SD) exerts its effect in cis or trans to Sd; and (6) if E(SD)+ exists, its function is not related to SD.

Animals↗
PubMed1984

Genetic studies of membrane excitability in Drosophila: lethal interaction between two temperature-sensitive paralytic mutations.

Two mutants of Drosophila melanogaster, parats1 (1-53.9) and napts (2-56.2) both display similar temperature-sensitive paralysis associated with blockage in the conduction of nerve action potentials, suggesting that the two gene products have a similar function. This idea is supported by the observation that the double mutant is unconditionally lethal. Genetic analysis of this synergistic interaction has revealed the following: it specifically involves the para and nap loci; all para alleles interact with napts, but the strength of the interaction varies in an allele-dependent fashion; lethality of the double mutant occurs during the first larval instar with parats1 but differs with other para alleles; hypodosage of para+ causes lethality in a napts background. These results together with previous electrophysiological, behavioral and pharmacological studies of these mutants suggest that both para and nap affect sodium channels and possibly encode different subunits.

Action Potentials↗
PubMed1983

Potassium currents in Drosophila: different components affected by mutations of two genes.

Electrophysiological analysis of the Drosophila behavioral mutants Eag and Sh and the double mutant Eag Sh indicates that the products of both genes take part in the control of potassium currents in the membranes of both nerve and muscle. In voltage-clamped larval muscle fibers, Sh affects the transient A current, whereas Eag reduces the delayed rectification and, to a lesser extent, the A current.

Action Potentials↗
PubMed1983

Neurogenetic analysis of potassium currents in Drosophila: synergistic effects on neuromuscular transmission in double mutants.

Recombinational dissection of the ShrK0120 strain of Drosophila melanogaster demonstrated that its extremely prolonged neuromuscular transmission, a defect qualitatively different from other Sh alleles, results from a synergistic interaction with a second site mutation. This new mutation caused spontaneous repetitive firing in motor axons and increased transmitter release. Complementation tests showed that it is allelic to eag. Combining either eag allele with various Sh alleles reproduced the same extreme defect observed in the original ShrK0120 strain. Thus, from their effects on neuromuscular transmission no qualitative difference among Sh alleles is apparent while Sh, eag, and eag Sh double mutant individuals can be uniquely distinguished. Pharmacological experiments indicated that Sh affects a membrane component sensitive to the potassium channel blockers 4-AP and TEA while eag affects a component sensitive to TEA but not 4-AP. We suggest that eag and Sh preferentially disrupt different potassium currents explaining their synergistic interaction.

Animals↗
PubMed1978

A Drosophila mutant with a temperature-sensitive block in nerve conduction.

A mutant, napts (no action potential, temperature-sensitive), is described in which axonal conduction fails at high temperature. Synaptic transmission at the larval neuromuscular junction is unimpaired. Larvae and adults are rapidly paralyzed at restrictive temperatures; they recover rapidly when the temperature is decreased. The mutant gene is recessive and is located on the second chromosome at map position 56.

Action Potentials↗
PubMed1977

On the components of segregation distortion in Drosophila melanogaster.

The segregation distorter (SD) complex is a naturally occurring meiotic drive system with the property that males heterozygous for an SD-bearing chromosome 2 and an SD(+)-bearing homolog transmit the SD-bearing chromosome almost exclusively. This distorted segregation is the consequence of an induced dysfunction of those sperm that receive the SD(+) homolog. From previous studies, two loci have been implicated in this phenomenon: the Sd locus which is required to produce distortion, and the Responder (Rsp) locus that is the site at which Sd acts. There are two allelic alternatives of Rsp-sensitive (Rsp(sens)) and insensitive (Rsp(ins)); a chromosome carrying Rsp(ins) is not distorted by SD. In the present study, the function and location of each of these elements was examined by a genetic and cytological characterization of X-ray-induced mutations at each locus. The results indicate the following: (1) the Rsp locus is located in the proximal heterochromatin of 2R; (2) a deletion for the Rsp locus renders a chromosome insensitive to distortion; (3) the Sd locus is located to the left of pr (2-54.5), in the region from 37D2-D7 to 38A6-B2 of the salivary chromosome map; (4) an SD chromosome deleted for Sd loses its ability to distort; (5) there is another important component of the SD system, E(SD), in or near the proximal heterochromatin of 2L, that behaves as a strong enhancer of distortion. The results of these studies allow a reinterpretation of results from earlier analyses of the SD system and serve to limit the possible mechanisms to account for segregation distortion.

Alleles↗