Developmental genetics of a lethal mutation, muscular dysgenesis (mdg), in the mouse

1965 ◽  
Vol 11 (1) ◽  
pp. 93-109 ◽  
Author(s):  
Anna C. Pai
1927 ◽  
Vol 61 (677) ◽  
pp. 520-530 ◽  
Author(s):  
R. A. Brink
Keyword(s):  

1956 ◽  
Vol 54 (2) ◽  
pp. 219-235 ◽  
Author(s):  
Walter Landauer
Keyword(s):  

Genetics ◽  
1979 ◽  
Vol 92 (1) ◽  
pp. 151-160
Author(s):  
H Traut

ABSTRACT When females of Drosophila melanogaster are treated with chemical or physical mutagens, not only in one but also in both of the two homologous X chromosomes of a given oocyte, a recessive sex-linked lethal mutation may be induced. A method is described that discriminates between such "single" and "double mutations." A theory is developed to show how a comparison between the expected and the observed frequency of double mutations yields an indication of the intercellular distribution (random or nonrandom) of recessive lethal mutations induced by mutagenic agents in oocytes and, consequently, of the distribution (homogeneous or nonhomogeneous) of those agents.—Three agents were tested: FUdR (12.5, 50.0 and 81.0,μg/ml), mitomycin C (130.0 μg/ml) and X rays (2000 R, 150 kV). After FUdR feeding, no increase in the mutation frequency usually observed in D. melanogaster without mutagenic treatment was obtained (u=0.13%, namely three single mutations among 2332 chromosomes tested). After mitomycin C feeding, 104. single and three double mutations were obtained. All of the 50 mutations observed after X irradiation were single mutations. The results obtained in the mitomycin C and radiation experiments favor the assumption of a random intercellular distribution of recessive lethal mutations induced by these two agents in oocytes of D. melanogaster. Reasons are discussed why for other types of mutagenic agents nonrandom distributions may be observed with our technique.


1992 ◽  
Vol 267 (34) ◽  
pp. 24625-24633
Author(s):  
A.H. West ◽  
D.J. Clark ◽  
J Martin ◽  
W Neupert ◽  
F.U. Hartl ◽  
...  

Genetics ◽  
1982 ◽  
Vol 101 (3-4) ◽  
pp. 461-476
Author(s):  
Todd R Laverty ◽  
J K Lim

ABSTRACT In this study, we show that at least one lethal mutation at the 3F-4A region of the X chromosome can generate an array of chromosome rearrangements, all with one chromosome break in the 3F-4A region. The mutation at 3F-4A (secondary mutation) was detected in an X chromosome carrying a reverse mutation of an unstable lethal mutation, which was mapped in the 6F1-2 doublet (primary mutation). The primary lethal mutation at 6F1-2 had occurred in an unstable chromosome (Uc) described previously (Lim 1979). Prior to reversion, the 6F1-2 mutation had generated an array of chromosome rearrangements, all having one break in the 6F1-2 doublet (Lim 1979, 1980). In the X chromosomes carrying the 3F-4A secondary lethal mutation the 6F1-2 doublet was normal and stable, as was the 3F-4A region in the X chromosome carrying the primary lethal mutation. The disappearance of the instability having a set of genetic properties at one region (6F1-2) accompanied by its appearance elsewhere in the chromosome (3F-4A) implies that a transposition of the destabilizing element took place. The mutant at 3F-4A and other secondary mutants exhibited all but one (reinversion of an inversion to the normal sequence) of the eight properties of the primary lethal mutations. These observations support the view that a transposable destabilizing element is responsible for the hypermutability observed in the unstable chromosome and its derivaties.


1970 ◽  
Vol 61 (5) ◽  
pp. 219-220 ◽  
Author(s):  
KATHARINE P. HUMMEL
Keyword(s):  

1977 ◽  
Vol 29 (1) ◽  
pp. 55-63 ◽  
Author(s):  
R. T. M. Poulter ◽  
N. K. Honey

SUMMARYThe homothallic amoebal clones of Physarum polycephalum are of potential use in understanding the developmental genetics of this organism. Such an application requires that complementation and recombination analysis be possible between pairs of homothallic clones. This paper is a report of the formation of mixed plasmodia by pairs of homothallic amoebal clones. In order to detect such mixed plasmodia use was made of two marker genes involved in plasmodial fusion, fusA and fusB. Sporulation of a mixed plasmodium formed from two homothallic (delayed) amoebal clones yielded progeny amoebae which were genetically recombinant. It is deduced from the ratios of various genotypes in these progeny clones that the mixed plasmodium was diploid and that meiosis was associated with sporulation. There is therefore no impediment to the use of the homothallic strains for genetical analysis. The progeny amoebal clones were observed to be showing segregation for the characters homothallic (rapid) and homothallic (delayed). This observation, taken together with other related observations, suggests that the homothallic (delayed) character is produced by mutation of the homothallic (rapid) character. The rare plasmodia formed by a homothallic (delayed) amoebal clone are the result of reversion of this mutation. Amoebal clones of the homothallic (delayed) type are therefore developmental mutants unable to perform the differentiation from amoeba to plasmodium.


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