The effects of translocations on recombination frequency in Caenorhabditis elegans.

Genetics ◽  
1988 ◽  
Vol 120 (4) ◽  
pp. 987-1001
Author(s):  
K S McKim ◽  
A M Howell ◽  
A M Rose

Abstract In the nematode Caenorhabditis elegans, recombination suppression in translocation heterozygotes is severe and extensive. We have examined the meiotic properties of two translocations involving chromosome I, szT1(I;X) and hT1(I;V). No recombination was observed in either of these translocation heterozygotes along the left (let-362-unc-13) 17 map units of chromosome I. Using half-translocations as free duplications, we mapped the breakpoints of szT1 and hT1. The boundaries of crossover suppression coincided with the physical breakpoints. We propose that DNA sequences at the right end of chromosome I facilitate pairing and recombination. We use the data from translocations of other chromosomes to map the location of pairing sites on four other chromosomes. hT1 and szT1 differed markedly in their effect on recombination adjacent to the crossover suppressed region. hT1 had no effect on recombination in the adjacent interval. In contrast, the 0.8 map unit interval immediately adjacent to the szT1(I;X) breakpoint on chromosome I increased to 2.5 map units in translocation heterozygotes. This increase occurs in a chromosomal interval which can be expanded by treatment with radiation. These results are consistent with the suggestion that the szT1(I) breakpoint is in a region of DNA in which meiotic recombination is suppressed relative to the genomic average. We propose that DNA sequences disrupted by the szT1 translocation are responsible for determining the frequency of meiotic recombination in the vicinity of the breakpoint.

Genetics ◽  
1990 ◽  
Vol 126 (2) ◽  
pp. 355-363
Author(s):  
M C Zetka ◽  
A M Rose

Abstract In the nematode Caenorhabditis elegans, hermaphrodite recombination has been characterized and is the basis of the genetic map used in this organism. In this study we have examined male recombination on linkage group I and have found it to be approximately one-third less than that observed in the hermaphrodite. This decrease was interval-dependent and nonuniform. We observed less recombination in the male in 5 out of 6 intervals examined, and no observable difference in one interval on the right end of LG I. Hermaphrodite recombination frequencies are the result of recombination in two germlines; oocyte and hermaphrodite spermatocytes. We have measured recombination in the oocyte and have found it to be approximately twofold lower than that calculated for hermaphrodite spermatocytes and not significantly different from the male spermatocyte frequency. Thus, recombination frequencies appear to be a function of gonad physiology rather than the sex of the germline. Evidence from experiments examining the effect of karyotype on recombination in males sexually transformed by the her-1 mutation into XO hermaphrodites (normally XX), suggests the sexual phenotype rather than genotype determines the recombination frequency characteristic of a particular sex. Hermaphrodite recombination is known to be affected by temperature, maternal age, and the rec-1 mutation. We have examined the effect of these parameters on recombination in the male and have found male recombination frequency increased with elevated temperatures and in the presence of Rec-1, and decreased with paternal age.


Genetics ◽  
1982 ◽  
Vol 102 (4) ◽  
pp. 725-736
Author(s):  
Teresa M Rogalski ◽  
Donald G Moerman ◽  
David L Baillie

ABSTRACT Five formaldehyde-induced deficiencies that uncover unc-22 IV, a gene affecting muscle structure in the nematode Caenorhabditis elegans were isolated and positioned. The largest deficiency, sDf2, extends in both directions from unc-22 and is approximately 1.0-2.0 map units in length. The other four deficiencies, sDf7, sDf8, sDf9 and sDf10, are all smaller than sDf2 and are located within the region uncovered by this deficiency. Thirty-seven ethyl methanesulfonate-induced lethal and sterile mutations linked to unc-22 were isolated and tested for complementation with sDf2. Nineteen lethal mutations failed to complement sDf2. Sixteen of these were further positioned by recombination mapping and also by deficiency mapping with sDf7, sDf8, sDf9 and sDf10. These sixteen mutations define 11 new essential genes in this region. Eight of the genes lie in a 0.9-map unit interval to the left of unc-22, whereas the three remaining genes lie in a region of about 0.2 map units to the right of unc-22. We believe that two of the essential genes identified in this study, let-56 and let-52, are the adjacent genes on either side of unc-22. The lethal mutations exhibit a wide range of terminal phenotypes: from first stage larva to sterile adult.


Genetics ◽  
1974 ◽  
Vol 77 (1) ◽  
pp. 95-104
Author(s):  
J E Sulston ◽  
S Brenner

ABSTRACT Chemical analysis and a study of renaturation kinetics show that the nematode, Caenorhabditis elegans, has a haploid DNA content of 8 x IO7 base pairs (20 times the genome of E. coli). Eighty-three percent of the DNA sequences are unique. The mean base composition is 36% GC; a small component, containing the rRNA cistrons, has a base composition of 51% GC. The haploid genome contains about 300 genes for 4s RNA, 110 for 5s RNA, and 55 for (18 + 28)S RNA.


Genetics ◽  
2000 ◽  
Vol 156 (4) ◽  
pp. 1603-1621
Author(s):  
Jason D Lieb ◽  
Carlos Ortiz de Solorzano ◽  
Enrique Garcia Rodriguez ◽  
Arthur Jones ◽  
Michael Angelo ◽  
...  

Abstract The dosage compensation machinery of Caenorhabditis elegans is targeted specifically to the X chromosomes of hermaphrodites (XX) to reduce gene expression by half. Many of the trans-acting factors that direct the dosage compensation machinery to X have been identified, but none of the proposed cis-acting X chromosome-recognition elements needed to recruit dosage compensation components have been found. To study X chromosome recognition, we explored whether portions of an X chromosome attached to an autosome are competent to bind the C. elegans dosage compensation complex (DCC). To do so, we devised a three-dimensional in situ approach that allowed us to compare the volume, position, and number of chromosomal and subchromosomal bodies bound by the dosage compensation machinery in wild-type XX nuclei and XX nuclei carrying an X duplication. The dosage compensation complex was found to associate with a duplication of the right 30% of X, but the complex did not spread onto adjacent autosomal sequences. This result indicates that all the information required to specify X chromosome identity resides on the duplication and that the dosage compensation machinery can localize to a site distinct from the full-length hermaphrodite X chromosome. In contrast, smaller duplications of other regions of X appeared to not support localization of the DCC. In a separate effort to identify cis-acting X recognition elements, we used a computational approach to analyze genomic DNA sequences for the presence of short motifs that were abundant and overrepresented on X relative to autosomes. Fourteen families of X-enriched motifs were discovered and mapped onto the X chromosome.


Genetics ◽  
2003 ◽  
Vol 165 (2) ◽  
pp. 929-934 ◽  
Author(s):  
Arnold B Barton ◽  
Yuping Su ◽  
Jacque Lamb ◽  
Dianna Barber ◽  
David B Kaback

Abstract The subtelomeric DNA sequences from chromosome I of Saccharomyces cerevisiae are shown to be inherently poor substrates for meiotic recombination. On the basis of these results and prior observations that crossovers near telomeres do not promote efficient meiosis I segregation, we suggest that subtelomeric sequences evolved to prevent recombination from occurring where it cannot promote efficient segregation.


Genetics ◽  
1986 ◽  
Vol 112 (3) ◽  
pp. 459-468
Author(s):  
Marisa Sebastiano ◽  
Marina D'Alessio ◽  
Paolo Bazzicalupo

ABSTRACT Using a screening procedure that is based on a histochemical stain for the enzyme β-glucuronidase, we have isolated several mutants of the nematode Caenorhabditis elegans affected in β-glucuronidase activity. All of the mutations fall into one complementation group and identify a new gene, gus-1, which has been mapped on the right arm of linkage group I (LG I), 1.1 map units to the left of unc-54. The mutants have no visible phenotype, and their viabilities and fertilities are unaffected. Linked revertants of two of the mutations have been isolated. They restore enzyme activity to almost wild-type levels; the β-glucuronidase that one of the revertants produces differs from that of the wild type. We propose that gus-1 is the structural locus for β-glucuronidase.


Genetics ◽  
1981 ◽  
Vol 97 (2) ◽  
pp. 261-279 ◽  
Author(s):  
Carl D Johnson ◽  
John G Duckett ◽  
Joseph G Culotti ◽  
Robert K Herman ◽  
Philip M Meneely ◽  
...  

ABSTRACT Within a set of five separable molecular forms of acetylcholinesterase found in the nematode Caenorhabditis elegans, previously reported differences in kinetic properties identify two classes, A and B, likely to be under separate genetic control. Using differences between these classes in sensitivity to inactivation by sodium deoxycholate, a screening procedure was devised to search for mutants affected only in class A forms. Among 171 previously isolated behavioral and morphological mutant strains examined by this procedure, one (PR946) proved to be of the expected type, exhibiting a selective deficiency of class A acetylcholinesterase forms. Although originally isolated because of its uncoordinated behavior, this strain was subsequently shown to harbor mutations in two genes; one in the previously identified gene unc-3, accounting for its behavior, and one in a newly identified gene, ace-1, accounting for its selective acetylcholinesterase deficiency. Derivatives homozygous only for the ace-1 mutation also lacked class A acetylcholinesterase forms, but were behaviorally and developmentally indistinguishable from wild type. The gene ace-1 has been mapped near the right end of the X chromosome. Gene dosage experiments suggest that it may be a structural gene for a component of class A acetylcholinesterase forms.


Genetics ◽  
1995 ◽  
Vol 141 (4) ◽  
pp. 1339-1349 ◽  
Author(s):  
M C Zetka ◽  
A M Rose

Abstract Meiotic crossovers are not randomly distributed along the chromosome. In Caenorhabditis elegans the central portions of the autosomes have relatively few crossovers compared to the flanking regions. We have measured the frequency of crossing over for several intervals across chromosome I in strains mutant for rec-1. The chromosome is approximately 50 map units in both wild-type and rec-1 homozygotes, however, the distribution of exchanges is very different in rec-1. Map distances expand across the gene cluster and contract near the right end of the chromosome, resulting in a genetic map more consistent with the physical map. Mutations in two other genes, him-6 and him-14, also disrupted the distribution of exchanges. Unlike rec-1, individuals homozygous for him-6 and him-14 had an overall reduction in the amount of crossing over accompanied by a high frequency of nondisjunction and reduced egg hatching. In rec-1; him-6 and rec-1; him-14 homozygotes the frequency of crossing over was characteristic of the Him mutant phenotype, whereas the distribution of the reduced number of exchanges was characteristic of the Rec-1 pattern. It appears that these gene products play a role in establishing the meiotic pattern of exchange events.


2018 ◽  
Author(s):  
Dmitriy Li ◽  
Marianne Rocl ◽  
Raif Yuecel ◽  
Alexander Lorenz

AbstractSchizosaccharomyces pombe, also known as fission yeast, is an established model for studying chromosome biological processes. Over the years research employing fission yeast has made important contributions to our knowledge about chromosome segregation during meiosis, as well as meiotic recombination and its regulation. Quantification of meiotic recombination frequency is not a straightforward undertaking, either requiring viable progeny for a genetic plating assay, or relying on laborious Southern blot analysis of recombination intermediates. Neither of these methods lends itself to high-throughput screens to identify novel meiotic factors. Here, we establish visual assays novel to Sz. pombe for characterizing chromosome segregation and meiotic recombination phenotypes. Genes expressing red, yellow, and/or cyan fluorophores from spore-autonomous promoters have been integrated into the fission yeast genomes, either close to the centromere of chromosome I to monitor chromosome segregation, or on the arm of chromosome III to form a genetic interval at which recombination frequency can be determined. The visual recombination assay allows straightforward and immediate assessment of the genetic outcome of a single meiosis by epi-fluorescence microscopy without requiring tetrad dissection. We also demonstrate that the recombination frequency analysis can be automatized by utilizing imaging flow cytometry to enable high-throughput screens. These assays have several advantages over traditional methods for analysing meiotic phenotypes.


Sign in / Sign up

Export Citation Format

Share Document