摘要:

AbstractThe Mexican axolotl (Ambystoma mexicanum) has enjoyed wide use in experimental embryology for over 100 yr. Its usefulness has been extended into the area of developmental genetics largely due to the contributions of R. Briggs and R. R. Humphrey at Indiana University. To date over 30 mutants have been described, almost all of which affect development. Some of these have been discovered in inbred strains while others have been uncovered in recent Mexican imports. These mutants can be subdivided into several major classes. Maternal effect mutations lead to deficiencies in informational, structural, or metabolic components of the egg essential to early development prior to the time at which the embryo's own genome becomes active. In contrast, the developmental lethals affect later stages in embryogenesis when both morphogenetic and biochemical events are determined exclusively by the genotype of the embryo. Most lead to death at about feeding stage. Some, the cell lethals, are believed to suffer from fundamental metabolic defects affecting all parts of the embryo. Others affect the development of specific organs or tissues. The developmental nonlethals also affect specific systems, but ones that are not essential to survival. Some affect the development and survival of pigment cells and these, along with isozyme variants, are useful as markers in developmental experiments.A number of the mutants have been studied in detail, but others scarcely at all. The purpose of this review is to bring them to the attention of all developmental biologists in the hope that their potential will be even more widely recognized.

ISSN:0192-253X    

DOI:10.1002/dvg.1020060102

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1985

数据来源: WILEY

摘要:

AbstractPulses of various durations at temperatures between 29 and 38°C were applied to developing larvae ofDrosophila melanogastercarrying the temperature‐sensitive cell‐lethal mutation1 (1)ts726. The results show that it is not possible to reduce the time required for the induction of abnormalities in the mutant by treating larvae with heat pulses at temperatures higher than 29°C. Instead, treatment with high temperature leads to fewer abnormalities than 29°C treatments. Furthermore with high temperature treatments, the mutation has less effect on viability than is seen at 29°C. It is suggested that1 (1)ts726leads to abnormalities and death by a temperature‐induced imbalance between different physiological or development events, rather than by interfering with the ability of the cell or the organism to withstand high temperature i

ISSN:0192-253X    

DOI:10.1002/dvg.1020060103

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1985

数据来源: WILEY

摘要:

AbstractProduction of trisomic‐3LDrosophila melanogasterhas allowed further investigation of compensated levels of gene expression in autosomal trisomies. We find that four enzyme loci on this arm produce diploid levels of gene product in trisomic‐3L larvae. For one of these genes, we show that all three alleles are expressed at similar levels. Two genes on 3L display dose‐dependent levels of gene product, and their location, relative to the four compensating loci, indicates that these two classes of genes are not regionally separated. In trisomic‐2R larvae, the level of enzyme produced from on 2R‐linked gene was dose dependent. In contrast, measurements of five loci on the X chromosome in metafemales (X trisomies) suggest that most genes are compensated in these individuals. Heat‐shock gene expression in trisomic‐3L salivary glands was qualitatively similar to diploids. The quantities of the small hsps (from the 67B cluster on 3L) suggest that these four genes respond independently to the trisomic condition; two produce compensated levels of protein, whereas the other two produce dose‐dependent levels of protein. The amount of hsp 83 produced in trisomies was similar to diploids (compensated). However, quantification of hsp 83 RNA showed that a dose‐dependent level of transcript was produced. This implies that hsp 83 compensation is controlled post

ISSN:0192-253X    

DOI:10.1002/dvg.1020060104

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1985

数据来源: WILEY

摘要:

AbstractThree stage‐specific cohesive systems operate inD. discoideum: VEG, elaborated by vegetative cells: AR, by aggregation competent cells; and PAR, by post aggregation stage cells. Previous study of a mutant strain JC‐5 had shown the stability of its PAR system (but not the AR) to be temperature sensitive. However, the phenotypic expression of this mutation termedCohA is complicated by the presence in that strain of a preexisting mutant geneRdeA, which accelerates developmental events generally and alters the pattern of morphogenesis. Genetic evidence presented here indicates that the two mutations have been separated by parasexual recombination yielding aCohA,RdeA+segregant class of which strain JC‐36 is a prototype.At the permissive temperature, JC‐36 follows a morphogenetic sequence like that of the wild type in respect to timing, morphogenetic pattern, and spore appearance. At the restrictive temperature, it forms normal aggregates at the usual time but exhibits two morphogenetic aberrancies during post aggregative development. First, fruit construction is arrested at a stage approximating the 16 hr “Bottle” stage of the wild type, though more squat and blunt tipped, and then the aggregate regresses. Cytodifferentiation into spores and stalk cells is also blocked. Second, a shift of slugs migrating normally at the permissive temperature to the restrictive causes the latter to disintegrate progressively as they leave clumps of cells behind them within the flattened sheath.JC‐36 cells developing at the restrictive temperature also exhibited a decrease in EDTA resistant cohesivity attributable on two grounds to the sensitivity of the PAR system. In addition, the disappearance of the AR system completed in the wild type by the Mexicanhat (18–19 hr) stage is indefinitely arrested at an intermediate

ISSN:0192-253X    

DOI:10.1002/dvg.1020060105

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1985

数据来源: WILEY

ISSN:0192-253X    

DOI:10.1002/dvg.1020060106

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1985

数据来源: WILEY

ISSN:0192-253X    

DOI:10.1002/dvg.1020060101

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1985

数据来源: WILEY