摘要:

The mutantno-bridge(nobKS49) has its name from a structural defect in the protocerebral bridge of the central complex. This rod-shaped neuropil innobKS49has a large gap at the sagittal midplane, with some of the missing material accumulated more laterally. Mutantnobflies have a reduced maximal and average walking speed. Leg coordination is disturbed during turning but not while walking straight. Motivation for walking is low and steps are small due to slow forward swinging of the legs. Flies spontaneously may pass into an autistic (and possibly spastic) state in which they can move their legs and even perform cleaning movements but do not walk or fly. They spontaneously recover if left undisturbed. Gynandromorph experiments place the focus of the walking defects into the head. Mutant flies have a reduced tendency to escape when mechanically stimulated. In a brightly lit arena they do not avoid a black square above the horizon and they are negatively phototactic. In tethered flight optomotor responses are normal but the amplitude of spontaneous torque modulations as well as the number of torque spikes are reduced. If a single black bar is slowly rotated around the fly, the normal response pattern is observed. It vanishes, however, at moderately fast angular velocity at which the wild type still is fully responsible. The behavioral defects support the notion that the protocerebral bridge is part of a higher center for the regulation of behavior.

ISSN:0167-7063    

DOI:10.3109/01677069209083444

出版商:Taylor&Francis    

年代:1992

数据来源: Taylor

摘要:

On the basis of behavioral interactions with mutations in a potassium channel gene ofDrosophila—Shaker (Sh)—we have isolated mutations in a new gene calledinebriated (ine).In a wildtype background,inemutants display no observable behavioral defects. However, in aShmutant background,inemutations cause downturned wings and an indented thorax. This distinctive phenotype is also exhibited by flies of other genotypes that cause extreme neuronal hyperexcitability. We utilized the potassium channel blocking drugs quinidine and dideoxy forskolin (DDF) to test the effects ofineon synaptic transmission. DDF andinemutations each potentiated the effects of quinidine on synaptic transmission, but neither had any observable effects in the absence of quinidine. Application of DDF toinemutants had no effects either in the presence or absence of quinidine. We conclude thatinemutations increase neuronal membrane excitability and perhaps block a DDF-sensitive potassium channel.

ISSN:0167-7063    

DOI:10.3109/01677069209083445

出版商:Taylor&Francis    

年代:1992

数据来源: Taylor

摘要:

TheClock (Clk)mutation shortens circadian rhythms of locomotor activity and eclosion from ca. 24 h to 22.5–23 h.Clkwas previously mapped, by meiotic recombination, very close to theperiod(per)locus on theXchromosome. To determine whetherClkis a mutation within thepergene or if the former is separate from the latter, two overlapping genomic fragments were cloned fromClkflies to produce aper-containing 13.2 kb construct,per01flies (which by themselves are arrhythmic)—when transformed with this construct—-expressed short-period rhythms. This indicates that theClkmutation is contained within this 13.2 kb region and is almost certainly a new“fast-clock”allele ofper.

ISSN:0167-7063    

DOI:10.3109/01677069209083446

出版商:Taylor&Francis    

年代:1992

数据来源: Taylor

摘要:

TheDrosophila pecanexlocus contains a maternal-effect neurogenic gene. A homologue of this gene has not yet been described in mammals or other organisms. We report here a partial complementary DNA clone from rat brain mRNA that encodes sequences which are very similar (83% over 189 amino acids) to a portion of sequence encoded by a transcript from theDrosophila pecanexlocus [LaBonne, S.G., Sunitha, I and Mahowald, A.P. (1989) Dev. Biology 136: 1–16].

ISSN:0167-7063    

DOI:10.3109/01677069209083447

出版商:Taylor&Francis    

年代:1992

数据来源: Taylor