Recessive Lethal Mutations and the Maintenance of Duplication-Bearing Strains of Dictyostelium discoideum

Genetics ◽  
1987 ◽  
Vol 115 (1) ◽  
pp. 101-106
Author(s):  
Dennis L Welker ◽  
Keith L Williams
Keyword(s):  
Linkage Group ◽  
Dictyostelium Discoideum ◽  
Chromosome Doubling ◽  
Chromosome Loss ◽  
New Mutation ◽  
Recessive Lethal ◽  
Lethal Mutations ◽  
Probable Gene ◽  
Subsequent Loss ◽  
Slow Growing

ABSTRACT Recessive lethal mutations have been isolated and used to maintain n + 1 aneuploid strains of Dictyostelium discoideum carrying a duplication of part or all of linkage group VII. The recessive lethal mutations, relA351 and relB352, arose spontaneously in diploids; no mutagenic treatment was used in the isolation of these mutations. The probable gene order on linkage group VII is: centromere, relB, couA, bsgB, cobA, relA . Maintenance of aneuploids disomic for linkage group VII was made possible by complementation of a rel mutation on each linkage group VII homologue by the corresponding wild-type allele on the other linkage group VII homologue. The duplication-bearing disomic strains were slow-growing and produced faster-growing sectors on the colony edge. Haploid sectors probably arise by a combination of mitotic recombination and subsequent loss of one homologue, diploid sectors may be formed by chromosome doubling to 2n + 2, followed by chromosome loss to return to 2n, and aneuploid sectors may arise by deletion or new mutation.

scholarly journals CHROMOSOME REARRANGEMENTS IN CAENORHABDITIS ELEGANS

Genetics ◽  
1976 ◽  
Vol 83 (1) ◽  
pp. 91-105
Author(s):  
Robert K Herman ◽  
Donna G Albertson ◽  
Sydney Brenner
Keyword(s):  
Linkage Group ◽  
Fluorescence Microscopy ◽  
The Other ◽  
Crossing Over ◽  
Group V ◽  
X Chromosomes ◽  
Recessive Lethal ◽  
C Elegans ◽  
Lethal Mutations ◽  
Chromosome Fragments

ABSTRACT A method for selecting unlinked duplications of a part of the X chromosome of C. elegans is described. Five such duplications have been identified. One of them, Dp(X;V)1, is translocated to linkage group V, where it suppresses crossing over along the left half of linkage group V. Dp(X;V)1 homozygotes grow slowly and are sterile. The other four duplications are associated with chromosome fragments, as observed cytologically by fluorescence microscopy, and tend to be lost. Their frequency of loss is higher in strains homozygous for a mutation that promotes nondisjunction of X chromosomes. The recombination frequencies between two of these duplications and the X have been measured: the frequencies are at least 50 times less than for X-X recombination in the same region. The duplications may prove useful as balancers of recessive lethal mutations.

scholarly journals Genomic organization in Caenorhabditis elegans: deficiency mapping on linkage group V(left)

1988 ◽  
Vol 52 (2) ◽  
pp. 105-118 ◽  
Author(s):  
Raja E. Rosenbluth ◽  
Teresa M. Rogalski ◽  
Robert C. Johnsen ◽  
Linda M. Addison ◽  
David L. Baillie
Keyword(s):  
Caenorhabditis Elegans ◽  
Linkage Group ◽  
Mutant Allele ◽  
Genomic Organization ◽  
Group V ◽  
Recessive Lethal ◽  
C Elegans ◽  
Lethal Mutations ◽  
Autosomal Region ◽  
Complementation Groups

SummaryIn this study we genetically analyse a large autosomal region (23 map units) in Caenorhabditis elegans. The region comprises the left half of linkage group V [LGV(left)] and is recombinationally balanced by the translocation eT1(III; V). We have used rearrangement breakpoints to subdivide the region from the left end of LGV to daf-11 into a set of 23 major zones. Twenty of these zones are balanced by eT1. To establish the zones we examined a total of 110 recessive lethal mutations derived from a variety of screening protocols. The mutations identified 12 deficiencies, 1 duplication, as well as 98 mutations that fell into 59 complementation groups, significantly increasing the number of available genetic sites on LGV. Twenty-six of the latter had more than 1 mutant allele. Significant differences were observed among the alleles of only 6 genes, 3 of which have at least one ‘visible’ allele. Several deficiencies and 3 alleles of let-336 were demonstrated to affect recombination. The duplication identified in this study is sDp30(V;X). Lethal mutations covered by sDp30 were not suppressed uniformly in hermaphrodites. The basis for this non-uniformity may be related to the mechanism of X chromosome dosage compensation in C. elegans.

scholarly journals CHROMOSOME REARRANGEMENTS IN DICTYOSTELIUM DISCOIDEUM

Genetics ◽  
1982 ◽  
Vol 102 (4) ◽  
pp. 711-723
Author(s):  
Dennis L Welker ◽  
Birgit A Metz ◽  
Keith L Williams
Keyword(s):  
Dna Damage ◽  
Dna Repair ◽  
Linkage Group ◽  
Dictyostelium Discoideum ◽  
Tandem Duplication ◽  
Linkage Groups ◽  
Group Iii ◽  
Radiation Resistant ◽  
Slow Growing ◽  
Multiple Recombination

ABSTRACT A tandem duplication (D350(III,III)) of the whiB to radB interval of linkage group III has been characterized. The gene order on the duplication-bearing chromosome is: centromere, whiB500, radB+, whiB+, radB24, bsgA5, acrC4. Slow-growing, duplication-bearing strains (yellow-spored, radiation-resistant) produced four classes of faster growing sectors involving the whiB and radB loci: white-spored, radiation-sensitive (whiB500, radB24); white-spored, radiation-resistant (whiB500, radB+); yellow-spored, radiation-sensitive (whiB+, radB24); and yellow-spored, radiation-resistant. The first three classes can be explained as the products of single recombination events in which one copy of the whiB to radB interval was lost. The yellow-spored, radiation-resistant sectors probably arose by mutation elsewhere in the genome, but alternatively may represent multiple recombination events or deletion of part of one copy of the duplicated region. Loss of the duplicated segment was enhanced by irradiation with ultraviolet light (254 nm). Heterozygosity for a DNA repair mutation at the radB locus may have been involved in the formation of the duplication. It is proposed that translocations are a major cause of nonrandom segregation patterns such as the cosegregation of unlinked markers in Dictyostelium discoideum. Translocations involving all known linkage groups are tabulated and DNA damage by N-methyl-N′-nitro-N-nitrosoguanidine is implicated in the formation of translocations in D. discoideum.

Maternal-effect lethal mutations on linkage group II of Caenorhabditis elegans.

Genetics ◽  
1988 ◽  
Vol 120 (4) ◽  
pp. 977-986
Author(s):  
K J Kemphues ◽  
M Kusch ◽  
N Wolf
Keyword(s):  
Caenorhabditis Elegans ◽  
Linkage Group ◽  
Maternal Effect ◽  
Essential Genes ◽  
The Other ◽  
C Elegans ◽  
Lethal Mutations ◽  
Embryonic Lethal ◽  
Embryonic Lethal Mutations ◽  
F1 Progeny

Abstract We have analyzed a set of linkage group (LG) II maternal-effect lethal mutations in Caenorhabditis elegans isolated by a new screening procedure. Screens of 12,455 F1 progeny from mutagenized adults resulted in the recovery of 54 maternal-effect lethal mutations identifying 29 genes. Of the 54 mutations, 39 are strict maternal-effect mutations defining 17 genes. These 17 genes fall into two classes distinguished by frequency of mutation to strict maternal-effect lethality. The smaller class, comprised of four genes, mutated to strict maternal-effect lethality at a frequency close to 5 X 10(-4), a rate typical of essential genes in C. elegans. Two of these genes are expressed during oogenesis and required exclusively for embryogenesis (pure maternal genes), one appears to be required specifically for meiosis, and the fourth has a more complex pattern of expression. The other 13 genes were represented by only one or two strict maternal alleles each. Two of these are identical genes previously identified by nonmaternal embryonic lethal mutations. We interpret our results to mean that although many C. elegans genes can mutate to strict maternal-effect lethality, most genes mutate to that phenotype rarely. Pure maternal genes, however, are among a smaller class of genes that mutate to maternal-effect lethality at typical rates. If our interpretation is correct, we are near saturation for pure maternal genes in the region of LG II balanced by mnC1. We conclude that the number of pure maternal genes in C. elegans is small, being probably not much higher than 12.

scholarly journals THE INTERCELLULAR DISTRIBUTION OF MUTATIONS INDUCED IN OOCYTES OF DROSOPHILA MELANOGASTER BY CHEMICAL AND PHYSICAL MUTAGENS

Genetics ◽  
1979 ◽  
Vol 92 (1) ◽  
pp. 151-160
Author(s):  
H Traut
Keyword(s):  
Drosophila Melanogaster ◽  
Mitomycin C ◽  
Mutation Frequency ◽  
Lethal Mutation ◽  
X Rays ◽  
Mutagenic Treatment ◽  
X Chromosomes ◽  
Recessive Lethal ◽  
Lethal Mutations ◽  
X Irradiation

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.

scholarly journals Cytogenetic and complementation analyses of recessive lethal mutations induced in the X chromosome of Drosophila by three alkylating agents

1974 ◽  
Vol 24 (1) ◽  
pp. 1-10 ◽  
Author(s):  
J. K. Lim ◽  
L. A. Snyder
Keyword(s):  
Drosophila Melanogaster ◽  
Salivary Gland ◽  
X Chromosome ◽  
Alkylating Agents ◽  
Complementation Analysis ◽  
Ethyl Methanesulphonate ◽  
Induced Mutations ◽  
Recessive Lethal ◽  
Lethal Mutations

SUMMARYSalivary-gland chromosomes of 54 methyl methanesulphonate- and 50 triethylene melamine-induced X-chromosome recessive lethals in Drosophila melanogaster were analysed. Two of the lethals induced by the mono-functional agent and 11 of those induced by the polyfunctional agent were found to be associated with detectable aberrations. A complementation analysis was also done on 82 ethyl methanesulphonate- and 34 triethylene melamine-induced recessive lethals in the zeste-white region of the X chromosome. The EMS-induced lethals were found to represent lesions affecting only single cistrons. Each of the 14 cistrons in the region known to mutate to a lethal state was represented by mutant alleles, but in widely different frequencies. Seven of the TEM-induced lethals were associated with deletions, only one of which had both breakpoints within the mapped region. Twenty-six of the 27 mutations in which only single cistrons were affected were mapped to 7 of the 14 known loci. One TEM- and two EMS-induced mutations were alleles representing a previously undetected locus in the zeste-white region.

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