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1. |
Mutants with Delayed Cell Death of the Ptilinal Head Muscles inDrosophila |
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Journal of Neurogenetics,
Volume 8,
Issue 2,
1992,
Page 57-69
IchiKen,
TanimuraTeiichi,
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摘要:
The emergence of adultDrosophila melanogasterfrom the puparium is followed by the programmed degeneration of a number of muscle groups. We have isolated two X-linked mutants that delay the programmed death of at least some of these muscles. During eclosion, the fly makes use of a membranous sac, the ptilinum, which is later retracted into the head capsule. Six of the eight sets of muscles involved in the retraction then undergo degeneration. The muscle fibers initially show a gradual atrophy and then degenerate rapidly through fragmentation followed by absorption. In wild-type flies, this degeneration is obvious by 12 h after eclosion due to the loss of the birefringence of the muscles. Through mutagenesis with ethyl methanesulfonate, we isolated four mutants whose birefringence of the doomed muscles was retained even at 12 h. Mutants were genetically classified into two complementation groups;mcd-1andmcd-2(mcd: muscle cell death). The muscles of themcd-1mutants degenerate more slowly than that of the wild-type flies; the fibers enter the fragmentation step but are then not rapidly absorbed. In themcd-2mutants, the fibers atrophy more slowly than that in the wild-type flies and fail to undergo fragmentation. The difference in the process of the muscle death between themcd-1and themcd-2mutants suggests that at least two genes act on different steps in the process of muscle cell death.
ISSN:0167-7063
DOI:10.3109/01677069209084152
出版商:Taylor&Francis
年代:1992
数据来源: Taylor
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2. |
Genetic and Age Related Models of Neurodegeneration in Mice: Dystrophic Axons |
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Journal of Neurogenetics,
Volume 8,
Issue 2,
1992,
Page 71-83
BronsonRoderick T.,
SweetHope O.,
SpencerCarole A.,
DavissonMuriel T.,
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摘要:
Dystrophic axons (DA) are non-specific lesions that occur in a wide variety of human and animal diseases. In this paper we describe the distribution of these lesions in three newly discovered mouse neurological mutants. The distribution of DA in these mutants is defined by their names, lumbosacral neuroaxonal dystrophy (lnd), located on Chromosome 7, generalized neuroaxonal dystrophy (gnd) and vestibulomotor degeneration (vmd). The last mutant, which has degeneration as well as DA in lateral vestibular nucleus and vestibulo-spinal tracts, dies in the first weeks of life; the first two live for approximately one year. A previously described mutation, dystonia musculorum (dt), was found to produce generalized DA likegnd, butdt/dtmutants die at an early age. DA were also found to occur in the nuclei gracilis and cuneatus, in the area of Clark's column and in lumbo-sacral spinal cord in aging normal mice either fed ad libitum or at a level of 40% dietary restriction. The dietary regimen had little effect on the numbers of DA observed in susceptible areas of the neuroaxis. The mutant models of neuroaxonal dystrophy may prove useful in studies of the pathophysiology of DA in general and of specific inherited diseases of man, such as infantile neuroaxonal dystrophy and Hallervordin-Spatz disease.
ISSN:0167-7063
DOI:10.3109/01677069209084153
出版商:Taylor&Francis
年代:1992
数据来源: Taylor
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3. |
Mutations on the Second Chromosome Affecting theDrosophilaEye |
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Journal of Neurogenetics,
Volume 8,
Issue 2,
1992,
Page 85-100
BakerNicholas E.,
MosesKevin,
NakaharaDonna,
EllisMichael C.,
CarthewRichard W.,
RubinGerald M.,
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摘要:
In the developing eye ofDrosophila, cell interactions appear to be responsible for organising undifferentiated cells into unit eyes, or ommatidia. Extensive mutagenesis has been used to search for mutations affecting the development and differentiation of ommatidia. These mutations have been characterized using sections of adults and immunocytochemistry of imaginal discs. Fourteen loci on the second chromosome are described that affect the spacing of the preclusters, the differentiation of ommatidial cells, orientation of the ommatidia, or architecture of the adult retina, that cause retinal degeneration in larval or pupal eye discs, or that cause homeotic transformation of part of the head.
ISSN:0167-7063
DOI:10.3109/01677069209084154
出版商:Taylor&Francis
年代:1992
数据来源: Taylor
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4. |
The Analysis of New Short-Period Circadian Rhythm Mutants Suggests Features ofD. Melanogaster PeriodGene Function |
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Journal of Neurogenetics,
Volume 8,
Issue 2,
1992,
Page 101-113
RutilaJoan E.,
EderyIsaac,
HallJeffrey C.,
RosbashMichael,
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摘要:
A number of newperiodgene (per) mutants were generated byin vitromutagenesis and germ line transformation. Missense mutations were made at amino acid 589, which is altered in the 19 h short-period (peras) mutant, and insertion mutations were generated with peptides commonly used for epitope tagging. Most of these newpermutants had short behavioral rhythms. Flies with heteroallelic combinations of these new mutantpergenes were found to have“hybrid”periods, i.e., they had values that were usually in between those of the individual alleles. These findings suggest that short-periodpermutants are not unusual gain-of-function mutants but rather more traditional loss-of-function mutants that are unable to influence the circadian pacemaker in a proper manner. The data also suggest that theperprotein may engage in important intermolecular interactions.
ISSN:0167-7063
DOI:10.3109/01677069209084155
出版商:Taylor&Francis
年代:1992
数据来源: Taylor
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5. |
Additive Gene Actions on the Fiber Number in the Anterior Optic Tract ofDrosophila Melanogaster |
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Journal of Neurogenetics,
Volume 8,
Issue 2,
1992,
Page 115-123
HoubéBernhard,
FriedrichKarl,
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摘要:
The influence of mutations in seven neurological genes on the number of fibers in the anterior optic tract (AOT) ofDrosophila melanogasterhas been investigated. It is shown that the number of fibers in the AOT can be drastically reduced in single and especially in multiple mutants. However, no evidence for synergistic interactions between the sample of mutations used in thesine oculis(so),reduced optic lobes(rol),minibrain(mnb), andsmall optic lobes(sol) genes was obtained at the level of the AOT. TherolKS222andsomutations eliminate similar fiber sets in the AOT, which are distinctly different from those eliminated bysolKS58andmnb1.
ISSN:0167-7063
DOI:10.3109/01677069209084156
出版商:Taylor&Francis
年代:1992
数据来源: Taylor
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