scholarly journals Two types of sites required for meiotic chromosome pairing in Caenorhabditis elegans.

Genetics ◽  
1993 ◽  
Vol 134 (3) ◽  
pp. 749-768 ◽  
Author(s):  
K S McKim ◽  
K Peters ◽  
A M Rose
Keyword(s):  
Caenorhabditis Elegans ◽  
Meiotic Chromosome ◽  
Chromosome Rearrangement ◽  
The Other ◽  
Crossing Over ◽  
Homologous Chromosomes ◽  
Associated Sequences ◽  
Suppressed Recombination ◽  
The Right ◽  
Chromosome I

Abstract Previous studies have shown that isolated portions of Caenorhabditis elegans chromosomes are not equally capable of meiotic exchange. These results led to the proposal that a homolog recognition region (HRR), defined as the region containing those sequences enabling homologous chromosomes to pair and recombine, is localized near one end of each chromosome. Using translocations and duplications we have localized the chromosome I HRR to the right end. Whereas the other half of chromosome I did not confer any ability for homologs to pair and recombine, deficiencies in this region dominantly suppressed recombination to the middle of the chromosome. These deletions may have disrupted pairing mechanisms that are secondary to and require an HRR. Thus, the processes of pairing and recombination appear to utilize at least two chromosomal elements, the HRR and other pairing sites. For example, terminal sequences from other chromosomes increase the ability of free duplications to recombine with their normal homologs, suggesting that telomere-associated sequences, homologous or nonhomologous, play a role in facilitating meiotic exchange. Recombination can also initiate at internal sites separated from the HRR by chromosome rearrangement, such as deletions of the unc-54 region of chromosome I. When crossing over was suppressed in a region of chromosome I, compensatory increases were observed in other regions. Thus, the presence of the HRR enabled recombination to occur but did not determine the distribution of the crossover events. It seems most likely that there are multiple initiation sites for recombination once homolog recognition has been achieved.

scholarly journals CROSSOVER SUPPRESSORS AND BALANCED RECESSIVE LETHALS IN CAENORHABDITIS ELEGANS

Genetics ◽  
1978 ◽  
Vol 88 (1) ◽  
pp. 49-65
Author(s):  
Robert K Herman
Keyword(s):  
Caenorhabditis Elegans ◽  
Linkage Group ◽  
The Other ◽  
Crossing Over ◽  
Linkage Groups ◽  
Recessive Lethal ◽  
X Ray ◽  
C Elegans ◽  
Complementation Groups ◽  
The Right

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.

scholarly journals Mutant rec-1 eliminates the meiotic pattern of crossing over in Caenorhabditis elegans.

Genetics ◽  
1995 ◽  
Vol 141 (4) ◽  
pp. 1339-1349 ◽  
Author(s):  
M C Zetka ◽  
A M Rose
Keyword(s):  
Caenorhabditis Elegans ◽  
Physical Map ◽  
Crossing Over ◽  
Gene Products ◽  
Wild Type ◽  
Egg Hatching ◽  
The Right ◽  
Chromosome I ◽  
Flanking Regions ◽  
Several Intervals

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.

scholarly journals The Role of Centromere Alignment in Meiosis I Segregation of Homologous Chromosomes in Saccharomyces cerevisiae

Genetics ◽  
1999 ◽  
Vol 153 (4) ◽  
pp. 1547-1560
Author(s):  
Cesar E Guerra ◽  
David B Kaback
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Chromosome Segregation ◽  
Meiotic Chromosome ◽  
Meiotic Spindle ◽  
Physical Interaction ◽  
Crossing Over ◽  
Homologous Chromosomes ◽  
Chromosome Alignment ◽  
Chromosome I

AbstractDuring meiosis, homologous chromosomes pair and then segregate from each other at the first meiotic division. Homologous centromeres appear to be aligned when chromosomes are paired. The role of centromere alignment in meiotic chromosome segregation was investigated in Saccharomyces cerevisiae diploids that contained one intact copy of chromosome I and one copy bisected into two functional centromere-containing fragments. The centromere on one fragment was aligned with the centromere on the intact chromosome while the centromere on the other fragment was either aligned or misaligned. Fragments containing aligned centromeres segregated efficiently from the intact chromosome, while fragments containing misaligned centromeres segregated much less efficiently from the intact chromosome. Less efficient segregation was correlated with crossing over in the region between the misaligned centromeres. Models that suggest that these crossovers impede proper segregation by preventing either a segregation-promoting chromosome alignment on the meiotic spindle or some physical interaction between homologous centromeres are proposed.

scholarly journals The meiotic behavior of an inversion in Caenorhabditis elegans.

Genetics ◽  
1992 ◽  
Vol 131 (2) ◽  
pp. 321-332 ◽  
Author(s):  
M C Zetka ◽  
A M Rose
Keyword(s):  
Caenorhabditis Elegans ◽  
Genetic Distance ◽  
Chiasma Formation ◽  
Crossing Over ◽  
Lethal Mutations ◽  
Meiotic Chromosomes ◽  
Entire Chromosome ◽  
The Right ◽  
Chromosome I ◽  
Segregation Of Chromosomes

Abstract The rearrangement hIn1(I) was isolated as a crossover suppressor for the right end of linkage group (LG) I. By inducing genetic markers on this crossover suppressor and establishing the gene order in the homozygote, hIn1(I) was demonstrated to be the first genetically proven inversion in Caenorhabditis elegans. hIn1(I) extensively suppresses recombination in heterozygotes in the right arm of chromosome I from unc-75 to unc-54. This suppression is associated with enhancement of recombination in other regions of the chromosome. The enhancement observed maintains the normal distribution of events but does not extend to other chromosomes. The genetic distance of chromosome I in inversion heterozygotes approaches 50 map units (m.u.), approximately equal to one chiasma per meiosis. This value is maintained in hIn1(I)/szT1(I;X) heterozygotes indicating that small homologous regions can pair and recombine efficiently. hIn1(I)/hT2(I;III) heterozygotes share no uninverted homologous regions and segregate randomly, suggesting the importance of chiasma formation in proper segregation of chromosomes. The genetic distance of chromosome I in these heterozygotes is less that 1 m.u., indicating that crossing over can be suppressed along an entire chromosome. Since one of our goals was to develop an efficient balancer for the right end of LGI, the effectiveness of hIn1(I) as a balancer was tested by isolating and maintaining lethal mutations. The meiotic behaviour of hIn1(I) is consistent with other genetic and cytogenetic data suggesting the meiotic chromosomes are monocentric. Rare recombinants bearing duplications and deficiencies of chromosome I were recovered from hIn1(I) heterozygotes, leading to the proposal the inversion was paracentric.

scholarly journals The Caenorhabditis elegans rol-6 gene, which interacts with the sqt-1 collagen gene to determine organismal morphology, encodes a collagen.

1990 ◽  
Vol 10 (5) ◽  
pp. 2081-2089 ◽  
Author(s):  
J M Kramer ◽  
R P French ◽  
E C Park ◽  
J J Johnson
Keyword(s):  
Caenorhabditis Elegans ◽  
Restriction Site ◽  
Genetic Interaction ◽  
The Other ◽  
C Elegans ◽  
Allele Specific ◽  
Specific Restriction ◽  
The Right ◽  
Sequence Similarities ◽  
Dominant Suppressor

The rol-6 gene is one of the more than 40 loci in Caenorhabditis elegans that primarily affect organismal morphology. Certain mutations in the rol-6 gene produce animals that have the right roller phenotype, i.e., they are twisted into a right-handed helix. The rol-6 gene interacts with another gene that affects morphology, sqt-1; a left roller allele of sqt-1 acts as a dominant suppressor of a right roller allele of rol-6. The sqt-1 gene has previously been shown to encode a collagen. We isolated and sequenced the rol-6 gene and found that it also encodes a collagen. The rol-6 gene was identified by physical mapping of overlapping chromosomal deficiencies that cover the gene and by identification of an allele-specific restriction site alteration. The amino acid sequence of the collagen encoded by rol-6 is more similar to that of the sqt-1 collagen than to any of the other ten C. elegans cuticle collagen sequences compared. The locations of cysteine residues flanking the Gly-X-Y repeat regions of rol-6 and sqt-1 are identical, but differ from those in the other collagens. The sequence similarities between rol-6 and sqt-1 indicate that they represent a new collagen subfamily in C. elegans. These findings suggest that these two collagens physically interact, possibly explaining the genetic interaction seen between the rol-6 and sqt-1 genes.

scholarly journals Crossing over is coupled to late meiotic prophase bivalent differentiation through asymmetric disassembly of the SC

2005 ◽  
Vol 168 (5) ◽  
pp. 683-689 ◽  
Author(s):  
Kentaro Nabeshima ◽  
Anne M. Villeneuve ◽  
Monica P. Colaiácovo
Keyword(s):  
Caenorhabditis Elegans ◽  
Symmetry Breaking ◽  
Synaptonemal Complex ◽  
Central Region ◽  
Meiotic Prophase ◽  
Homologous Chromosome ◽  
Meiotic Chromosome ◽  
Crossing Over ◽  
Γ Irradiation ◽  
Irradiation Treatment

Homologous chromosome pairs (bivalents) undergo restructuring during meiotic prophase to convert a configuration that promotes crossover recombination into one that promotes bipolar spindle attachment and localized cohesion loss. We have imaged remodeling of meiotic chromosome structures after pachytene exit in Caenorhabditis elegans. Chromosome shortening during diplonema is accompanied by coiling of chromosome axes and highly asymmetric departure of synaptonemal complex (SC) central region proteins SYP-1 and SYP-2, which diminish over most of the length of each desynapsing bivalent while becoming concentrated on axis segments distal to the single emerging chiasma. This and other manifestations of asymmetry along chromosomes are lost in synapsis-proficient crossover-defective mutants, which often retain SYP-1,2 along the full lengths of coiled diplotene axes. Moreover, a γ-irradiation treatment that restores crossovers in the spo-11 mutant also restores asymmetry of SYP-1 localization. We propose that crossovers or crossover precursors serve as symmetry-breaking events that promote differentiation of subregions of the bivalent by triggering asymmetric disassembly of the SC.

scholarly journals MAPPING AND GENE CONVERSION STUDIES WITH THE STRUCTURAL GENE FOR ISO-1-CYTOCHROME C IN YEAST

Genetics ◽  
1975 ◽  
Vol 81 (4) ◽  
pp. 615-629
Author(s):  
Christopher W Lawrence ◽  
Fred Sherman ◽  
Mary Jackson ◽  
Richard A Gilmore
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Gene Conversion ◽  
The Other ◽  
Crossing Over ◽  
Wild Type ◽  
Chromosome X ◽  
Tetrad Analysis ◽  
Yeast Saccharomyces Cerevisiae ◽  
Distal Marker ◽  
The Right

ABSTRACT We have investigated the order of the four genes cyc1, rad7, SUP4, and cdc8 which form a tightly linked cluster on the right arm of chromosome X in the yeast Saccharomyces cerevisiae. Crossing over and coconversion data from tetrad analysis established the gene order to be centromere–cyc1–rad7–SUP4. Also cdc8 appeared to be distal to SUP4 on the basis of crossovers that were associated with conversion of SUP4. The frequencies of recombination and the occurrence of coconversions suggest that these four genes are contiguous or at least nearly so. Gene-conversion frequencies for several cyc1 alleles were studied, including cyc1–1, a deletion of the whole gene that extends into the rad7 locus. The cyc1–1 deletion was found to be capable of conversion, though at a frequency some fivefold less than the other alleles studied, and both 3:1 and 1:3 events were detected. In general 1:3 and 3:1 conversion events were equally frequent at all loci studied, and approximately 50% of conversions were accompanied by reciprocal recombination for flanking markers. The orientation of the cyc1 gene could not be clearly deduced from the behavior of the distal marker SUP4 in wild-type recombinants that arose from diploids heteroallelic for cyc1 mutations.

scholarly journals Condensin restructures chromosomes in preparation for meiotic divisions

2004 ◽  
Vol 167 (4) ◽  
pp. 613-625 ◽  
Author(s):  
Raymond C. Chan ◽  
Aaron F. Severson ◽  
Barbara J. Meyer
Keyword(s):  
Caenorhabditis Elegans ◽  
Chromosome Segregation ◽  
Germ Cells ◽  
Protein Complex ◽  
Mitotic Chromosome ◽  
Meiotic Chromosome ◽  
Ordered Structure ◽  
Homologous Chromosomes ◽  
Sister Chromatids ◽  
Chromosome Resolution

The production of haploid gametes from diploid germ cells requires two rounds of meiotic chromosome segregation after one round of replication. Accurate meiotic chromosome segregation involves the remodeling of each pair of homologous chromosomes around the site of crossover into a highly condensed and ordered structure. We showed that condensin, the protein complex needed for mitotic chromosome compaction, restructures chromosomes during meiosis in Caenorhabditis elegans. In particular, condensin promotes both meiotic chromosome condensation after crossover recombination and the remodeling of sister chromatids. Condensin helps resolve cohesin-independent linkages between sister chromatids and alleviates recombination-independent linkages between homologues. The safeguarding of chromosome resolution by condensin permits chromosome segregation and is crucial for the formation of discrete, individualized bivalent chromosomes.

scholarly journals Excess crossovers impede faithful meiotic chromosome segregation in C. elegans

2020 ◽  
Author(s):  
Jeremy A. Hollis ◽  
Marissa L. Glover ◽  
Aleesa Schlientz ◽  
Cori K. Cahoon ◽  
Bruce Bowerman ◽  
...  
Keyword(s):  
Caenorhabditis Elegans ◽  
Chromosome Segregation ◽  
High Frequency ◽  
Meiotic Chromosome ◽  
Dependent Manner ◽  
Homologous Chromosomes ◽  
Crossover Interference ◽  
C Elegans ◽  
Functional Consequences ◽  
Chromosome Bridges

AbstractDuring meiosis, at least one crossover must form between each pair of homologous chromosomes to ensure their proper partitioning. However, most organisms limit the number of crossovers by a phenomenon called crossover interference; why this occurs is not well understood. Here we investigate the functional consequences of extra crossovers in Caenorhabditis elegans. Using a fusion chromosome that exhibits a high frequency of supernumerary crossovers, we find that essential chromosomal structures are mispatterned, subjecting chromosomes to improper spindle forces and leading to congression and segregation defects. Moreover, we uncover mechanisms that counteract these errors; anaphase I chromosome bridges were often able to resolve in a LEM-3 nuclease dependent manner, and tethers between homologs that persisted were frequently resolved during Meiosis II by a second mechanism. This study thus provides evidence that excess crossovers impact chromosome patterning and segregation, and also sheds light on how these errors are corrected.

scholarly journals Synaptonemal complex proteins direct and constrain the localization of crossover-promoting proteins during Caenorhabditis elegans meiosis

2019 ◽  
Author(s):  
Cori K. Cahoon ◽  
Jacquellyn M. Helm ◽  
Diana E. Libuda
Keyword(s):  
Caenorhabditis Elegans ◽  
Synaptonemal Complex ◽  
Meiotic Chromosome ◽  
Variable Number ◽  
Specific Structure ◽  
Dna Breaks ◽  
Late Prophase ◽  
Homologous Chromosomes ◽  
Sister Chromatids ◽  
Double Strand Dna Breaks

AbstractCrossovers (COs) between homologous chromosomes are critical for meiotic chromosome segregation and form in the context of the synaptonemal complex (SC), a meiosis-specific structure that assembles between aligned homologs. During Caenorhabditis elegans meiosis, central region components of the SC (SYP proteins) are essential to repair double-strand DNA breaks (DSBs) as COs, but the roles of these SYP proteins in promoting CO formation are poorly understood. Here, we investigate the relationships between the SYP proteins and conserved CO-promoting factors by examining the immunolocalization of these factors in meiotic mutants where SYP proteins are absent, reduced, or mis-localized. Although COs do not form in syp null mutants, CO-promoting proteins COSA-1, MSH-5, and ZHP-3 nevertheless become co-localized at a variable number of DSB-dependent sites during late prophase, reflecting an inherent affinity of these factors for DSB repair sites. In contrast, in mutants where SYP proteins are present but form aggregates or display abnormal synapsis, CO-promoting proteins consistently track with SYP-1 localization. Moreover, CO-promoting proteins usually localize to a single site per SYP-1 structure, even in SYP aggregates or in mutants where SC forms between sister-chromatids, suggesting that CO regulation occurs within these structures. Further, we find that sister chromatids in the meiotic cohesin mutant rec-8 require both CO-promoting proteins and the SC to remain connected. Taken together, our findings support a model in which SYP proteins promote CO formation by directing and constraining the localization of CO-promoting factors to ensure that CO maturation occurs only between properly aligned homologous chromosomes.Article SummaryErrors during meiosis are the leading cause of birth defects and miscarriages in humans. Thus, the coordinated control of meiosis events is critical for the faithful inheritance of the genome each generation. The synaptonemal complex (SC) is a meiosis-specific structure that assembles between homologs chromosomes and is critical for the establishment and regulation of crossovers, which ensure the accurate segregation of the homologous chromosomes at meiosis I. Here we show that the SC proteins function to regulate crossovers by directing and constraining the localization of proteins involved in promoting the formation of crossovers.

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