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

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.

Genetics ◽  
1978 ◽  
Vol 88 (1) ◽  
pp. 49-65
Author(s):  
Robert K Herman

ABSTRACT Two dominant suppressors of crossing over have been identified following X-ray treatment of the small nematode C. elegans. They suppress crossing over in linkage group II (LGII) about 100-fold and 50-fold and are both tightly linked to LGII markers. One, called C1, segregates independently of all other linkage groups and is homozygous fertile. The other is a translocation involving LGII and X. The translocation also suppresses rrossing over along the right half of X and is homozygous lethal. CI has been used as a balancer of LGII recessive lethal and sterile mutations induced by EMS. The frequencies of occurrence of lethals and steriles were approximately equal. Fourteen mutations were assigned to complementation groups and mapped. They tended to map in the same region where LGII visibles are clustered.


Genetics ◽  
1976 ◽  
Vol 83 (1) ◽  
pp. 91-105
Author(s):  
Robert K Herman ◽  
Donna G Albertson ◽  
Sydney Brenner

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.


Genetics ◽  
1988 ◽  
Vol 120 (4) ◽  
pp. 977-986
Author(s):  
K J Kemphues ◽  
M Kusch ◽  
N Wolf

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.


Genome ◽  
1990 ◽  
Vol 33 (1) ◽  
pp. 109-114 ◽  
Author(s):  
Denise V. Clark ◽  
Robert C. Johnsen ◽  
Kim S. McKim ◽  
David L. Baillie

A screen was conducted for lethal mutations in the nematode Caenorhabditis elegans in a strain containing the mutator mut-4(st700)I to examine the nature of mutator-induced lethal mutations within two large chromosomal regions comprising a total of 49 map units (linkage group IV (right) and linkage group V (left)). The genetic analysis of 28 lethal mutations has revealed that the mutator locus mut-4(st700)I causes both putative single-gene mutations and deficiencies. We have identified lethal mutations in three different genes, in addition to seven deficiencies. There is a mutational hot spot on linkage group V (left) around the lin-40 locus. Six mutations appear to be alleles of lin-40. In addition, 5 of 7 deficiencies have breakpoints at or very near lin-40. All seven deficiencies delete the left-most known gene on linkage group V (left) and thus appear to delete the tip of the chromosome. This is in contrast to gamma ray and formaldehyde induced deficiencies, which infrequently delete the closest known gene to the tip of a chromosome.Key words: Caenorhabditis elegans, mutator, deficiencies, lethal mutations.


Genetics ◽  
1988 ◽  
Vol 119 (2) ◽  
pp. 345-353
Author(s):  
D V Clark ◽  
T M Rogalski ◽  
L M Donati ◽  
D L Baillie

Abstract The organization of essential genes in the unc-22 region, defined by the deficiency sDf2 on linkage group IV, has been studied. Using the balancer nT1 (IV;V), which suppresses recombination over 49 map units, 294 lethal mutations on LGIV(right) and LGV(left) were recovered using EMS mutagenesis. Twenty-six of these mutations fell into the unc-22 region. Together with previously isolated lethal mutations, there is now a total of 63 lethal mutations which fall into 31 complementation groups. Mutations were positioned on the map using eight overlapping deficiencies in addition to sDf2. The lethal alleles and deficiencies in the unc-22 region were characterized with respect to their terminal phenotypes. Mapping of these lethal mutations shows that sDf2 deletes a minimum of 1.8 map units and a maximum of 2.5 map units. A minimum estimate of essential gene number for the region using a truncated Poisson calculation is 48. The data indicate a minimum estimate of approximately 3500 essential genes in the Caenorhabditis elegans genome.


1987 ◽  
Vol 49 (3) ◽  
pp. 207-213 ◽  
Author(s):  
A. M. Howell ◽  
S. G. Gilmour ◽  
R. A. Mancebo ◽  
A. M. Rose

SummaryIn this paper we describe the use of a free duplication, sDp2 (I;f), for the recovery, maintenance, and analysis of mutations defining essential genes in the left third of Linkage Group I of Caenorhabditis elegans. The lethals were induced in a strain of genotype (sDp2) + /dpy-5 + unc-13/ dpy-5 unc-15 +, using either 12 mM ethylmethane sulphonate or 1500 r of gamma radiation. Lethal mutations linked to the dpy-5 unc-13 chromosome were recognized by the absence of Dpy-5 Unc-13 individuals amongst the self progeny and were maintained by isolating Unc-13 hermaphrodites. These strains – which have two mutant alleles of the essential gene and a wild-type allele on the duplication – are balanced, since crossing-over does not occur between sDp2 and the normal homologues. Using this sytem we have recovered 58 EMS-induced mutations. These have been characterized with regard to map position and complementation. Twenty-nine of the EMS-induced mutations lie to the left of dpy-5 and define 20 complementation groups; 3 were inseparable from dpy-5 and define 3 complementation groups; 21 were to the right and define 17 complementation groups. Among a set of 29 gamma radiation-induced lethal mutations, 17 appear to be single gene mutations or are very small deletions. We estimate that we have identified from one-sixth to one-half of the essential genes in the sDp2 region.


Genome ◽  
1993 ◽  
Vol 36 (4) ◽  
pp. 712-724 ◽  
Author(s):  
Dave Pilgrim

A genetic approach was taken to identify new transposable element Tc1 -dependent polymorphisms on the left end of linkage group III in the nematode Caenorhabditis elegans. The cloning of the genomic DNA surrounding the Tc1 allowed the selection of overlapping clones (from the collection being used to assemble the physical map of the C. elegans genome). A contig of approximately 600–800 kbp in the region has been identified, the genetic map of the region has been refined, and 10 new RFLPs as well as at least four previously characterized genetic loci have been positioned onto the physical map, to the resolution of a few cosmids. This analysis demonstrated the ability to combine physical and genetic mapping for the rapid analysis of large genomic regions (0.5–1 Mbp) in genetically amenable eukaryotes.Key words: Caenorhabditis elegans, genome analysis, RFLP, physical map, genetic map.


1998 ◽  
Vol 260 (2-3) ◽  
pp. 280-288 ◽  
Author(s):  
H. I. Stewart ◽  
N. J. O'Neil ◽  
D. L. Janke ◽  
N. W. Franz ◽  
H. M. Chamberlin ◽  
...  

Genetics ◽  
1984 ◽  
Vol 108 (2) ◽  
pp. 331-345
Author(s):  
D Christine Sigurdson ◽  
Gail J Spanier ◽  
Robert K Herman

ABSTRACT Six schemes were used to identify 80 independent recessive lethal deficiencies of linkage group (LG) II following X-ray treatment of the nematode Caenorhabditis elegans. Complementation tests between the deficiencies and ethyl methanesulfonate-induced recessive visible, lethal and sterile mutations and between different deficiencies were used to characterize the extents of the deficiencies. Deficiency endpoints thus helped to order 36 sites within a region representing about half of the loci on LG II and extending over about 5 map units. New mutations occurring in this region can be assigned to particular segments of the map by complementation tests against a small number of deficiencies; this facilitates the assignment of single-site mutations to particular genes, as we illustrate. Five sperm-defective and five oocyte-defective LG II sterile mutants were identified and mapped. Certain deficiency-by-deficiency complementation tests allowed us to suggest that the phenotypes of null mutations at two loci represented by visible alleles are wild type and that null mutations at a third locus confer a visible phenotype. A segment of LG II that is about 12 map units long and largely devoid of identified loci seems to be greatly favored for crossing over.


Genetics ◽  
1987 ◽  
Vol 117 (3) ◽  
pp. 467-476
Author(s):  
Samuel M Politz ◽  
Karl J Chin ◽  
Daniel L Herman

ABSTRACT We have studied developmental stage-specificity and genetic specification of surface antigens in the nematode Caenorhabditis elegans. Rabbit antisera directed against the adult C. elegans cuticle were used in conjunction with antiserum adsorption experiments to obtain antibody reagents with specificity for the adult surface. Adult-specific antibodies were used to identify several varietal strains of C. elegans that display antigen-negative phenotypes as adults. Genetic mapping results using the surface antigen phenotype as a marker indicated that a single gene (designated srf-1) or cluster of genes on linkage group II determines the adult surface antigen phenotype.


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