Concluding remarks

Professor Darlington opened the meeting by challenging us with the view that chromosomes made the laws of heredity, rather than heredity fashioning the organization of chromosomes. To keep this wheel of logic spinning, it may be said that chromosomes also made the process of meiosis and thus determined the laws of meiotic exchange. I choose this gambit because our discussions lent considerable emphasis to the view that chromosome complexity compels its own sets of distinctive, and perhaps varied, mechanisms to effect the ultimate event of molecular recombination. The complexity that leads molecular recombination to operate in elaborate meiotic moulds is not, it should be emphasized, base sequence complexity. On the contrary, sequence repeats and genetic homoeologies, though adding disproportionately little to the base sequence complexity of a genome, adds considerably to the complexity of effecting chromosome alignment and crossing over. How chromosomes of diverse genetic content manage that complexity and in the process mould the characteristics of meiotic behaviour has been the primary target of our deliberations. That no single pattern of meiotic conduct was perceived in consequence of the discussions, is to be expected. To the extent that genomes differ in various aspects of chromosome organization - and that they do is patent - the particulars of meiotic organization might also differ. Although a strong sentiment was occasionally expressed for a single universal process of meiosis, it is my opinion that sameness and universality may be mistakenly treated as synonyms. Universals provide for diversity; they do not impose sameness. The task of identifying universal threads among different meiotic fabrics is not a straightforward one. The ultimate act of genetic recombination offers no detailed guide to the routes by which it may be achieved. Indeed, it is the structure of the chromosome that dictates the route ; recombination only signals the direction.

1970 ◽  
Vol 6 (3) ◽  
pp. 669-678
Author(s):  
B. C. LU

The frequency of genetic recombination in Coprinus lagopus may be modified by heat and cold shock. By removal of samples from a fruiting body before and after temperature treatment, it is possible to study the ultrastructure of chromosomes at the time recombination frequency (between den+ x +me-1) can be modified. The sensitive period for temperature effects and, therefore, probably the time of crossing over, commences with the formation of the synaptinemal complex (S.C.) and ends with its disappearance, i.e. during the entire existence of the S.C. It is concluded that recombination is an event subsequent to the formation of the S.C. and is independent of the process of its formation. It is suggested that the event takes place at the synaptic centre.


2018 ◽  
Vol 217 (10) ◽  
pp. 3343-3353 ◽  
Author(s):  
Sara Carvalhal ◽  
Alexandra Tavares ◽  
Mariana B. Santos ◽  
Mihailo Mirkovic ◽  
Raquel A. Oliveira

Sister chromatid cohesion mediated by cohesin is essential for mitotic fidelity. It counteracts spindle forces to prevent premature chromatid individualization and random genome segregation. However, it is unclear what effects a partial decline of cohesin may have on chromosome organization. In this study, we provide a quantitative analysis of cohesin decay by inducing acute removal of defined amounts of cohesin from metaphase-arrested chromosomes. We demonstrate that sister chromatid cohesion is very resistant to cohesin loss as chromatid disjunction is only observed when chromosomes lose >80% of bound cohesin. Removal close to this threshold leads to chromosomes that are still cohered but display compromised chromosome alignment and unstable spindle attachments. Partial cohesin decay leads to increased duration of mitosis and susceptibility to errors in chromosome segregation. We propose that high cohesin density ensures centromeric chromatin rigidity necessary to maintain a force balance with the mitotic spindle. Partial cohesin loss may lead to chromosome segregation errors even when sister chromatid cohesion is fulfilled.


2003 ◽  
Vol 23 (3) ◽  
pp. 873-886 ◽  
Author(s):  
Juan Lucas Argueso ◽  
Amanda Wraith Kijas ◽  
Sumeet Sarin ◽  
Julie Heck ◽  
Marc Waase ◽  
...  

ABSTRACT In eukaryotic cells, DNA mismatch repair is initiated by a conserved family of MutS (Msh) and MutL (Mlh) homolog proteins. Mlh1 is unique among Mlh proteins because it is required in mismatch repair and for wild-type levels of crossing over during meiosis. In this study, 60 new alleles of MLH1 were examined for defects in vegetative and meiotic mismatch repair as well as in meiotic crossing over. Four alleles predicted to disrupt the Mlh1p ATPase activity conferred defects in all functions assayed. Three mutations, mlh1-2, -29, and -31, caused defects in mismatch repair during vegetative growth but allowed nearly wild-type levels of meiotic crossing over and spore viability. Surprisingly, these mutants did not accumulate high levels of postmeiotic segregation at the ARG4 recombination hotspot. In biochemical assays, Pms1p failed to copurify with mlh1-2, and two-hybrid studies indicated that this allele did not interact with Pms1p and Mlh3p but maintained wild-type interactions with Exo1p and Sgs1p. mlh1-29 and mlh1-31 did not alter the ability of Mlh1p-Pms1p to form a ternary complex with a mismatch substrate and Msh2p-Msh6p, suggesting that the region mutated in these alleles could be responsible for signaling events that take place after ternary complex formation. These results indicate that mismatches formed during genetic recombination are processed differently than during replication and that, compared to mismatch repair functions, the meiotic crossing-over role of MLH1 appears to be more resistant to mutagenesis, perhaps indicating a structural role for Mlh1p during crossing over.


Genetics ◽  
1983 ◽  
Vol 103 (2) ◽  
pp. 161-178
Author(s):  
Helen Sang ◽  
Harold L K Whitehouse

ABSTRACT Aberrant asci containing one or more wild-type spores were selected from crosses between pairs of alleles of the buff locus in the presence of closely linked flanking markers. Data were obtained relating to the site of aberrant segregation and the position of any associated crossover giving recombination of flanking markers. Aberrant segregation at a proximal site within the buff gene may be associated with a crossover proximal to the site of aberrant segregation or, with equal frequency, with a crossover distal to the site of the second mutant present in the cross. Similarly, segregation at a distal site may be associated with a crossover distal to the site or, with lower frequency, with a crossover proximal to the site of the proximal mutant present in the cross. Crossovers between the alleles were rare. This evidence for the relationship between hybrid DNA and crossing over is discussed in terms of current models for the mechanism of recombination.


2019 ◽  
Author(s):  
Nikhil R Bhagwat ◽  
Shannon Owens ◽  
Masaru Ito ◽  
Jay Boinapalli ◽  
Philip Poa ◽  
...  

Protein modification by SUMO helps orchestrate the elaborate events of meiosis to faithfully produce haploid gametes. To date, only a handful of meiotic SUMO targets have been identified. Here we delineate a multidimensional SUMO-modified meiotic proteome in budding yeast, identifying 2747 conjugation sites in 775 targets, and defining their relative levels and dynamics. Modified sites cluster in disordered regions and only a minority match consensus motifs. Target identities and modification dynamics imply that SUMOylation regulates all levels of chromosome organization and each step of homologous recombination. Execution-point analysis confirms these inferences, revealing functions for SUMO in S-phase, the initiation of recombination, chromosome synapsis and crossing over. K15-linked SUMO chains become prominent as chromosomes synapse and recombine, consistent with roles in these processes. SUMO also modifies ubiquitin, forming hybrid oligomers with potential to modulate ubiquitin signaling. We conclude that SUMO plays diverse and unanticipated roles in regulating meiotic chromosome metabolism.


Genetics ◽  
1973 ◽  
Vol 75 (2) ◽  
pp. 231-246
Author(s):  
T K Fu ◽  
E R Sears

ABSTRACT Telocentrics for the β arm of chromosome 4A and the long arm of 6B were used as cytological markers for the determination of chiasma frequency. In concomitant studies of recombination, terminal segments of rye and T. umbellulatum chromatin carrying Hp (Hairy peduncle) and Lr9 (Leaf-rust resistance), respectively, marked 4A and 6B. Two temperatures, 21° and 32°, were used for both the 4A and 6B experiments.—Only one chiasma was observed in each heteromorphic bivalent. Because there was a substantial reduction in pairing between diakinesis and metaphase I, all determinations of chiasma frequency were made at diakinesis. In the 21° experiments, agreement was good between genetic recombination and cytological prediction on the basis of the partial chiasmatypy hypothesis that each chiasma represents a crossover. At 32° both chiasma frequency and crossing over, but particularly the latter, were strongly reduced. The fewer crossovers than expected are explained in part by stickiness of chromosomes at the high temperature, sometimes resulting in adjacent chromosomes being wrongly scored as having a chiasma, and in part by premetaphase disjunction of some recombined bivalents and subsequent independent behavior of the two resulting univalents.—Male transmission of the 4A telocentric from the heteromorphic bivalent was unusually high: 51% at 21° and 31% at 32°.


Cell ◽  
1975 ◽  
Vol 4 (2) ◽  
pp. 121-129 ◽  
Author(s):  
M.J. Getz ◽  
G.D. Birnie ◽  
B.D. Young ◽  
Elizabeth MacPhail ◽  
J. Paul

2020 ◽  
Vol 14 (12) ◽  
pp. e0008945
Author(s):  
Hampate Ba ◽  
Sarah Auburn ◽  
Christopher G. Jacob ◽  
Sonia Goncalves ◽  
Craig W. Duffy ◽  
...  

Background Plasmodium vivax has been recently discovered as a significant cause of malaria in Mauritania, although very rare elsewhere in West Africa. It has not been known if this is a recently introduced or locally remnant parasite population, nor whether the genetic structure reflects epidemic or endemic transmission. Methodology/Principal findings To investigate the P. vivax population genetic structure in Mauritania and compare with populations previously analysed elsewhere, multi-locus genotyping was undertaken on 100 clinical isolates, using a genome-wide panel of 38 single nucleotide polymorphisms (SNPs), plus seven SNPs in drug resistance genes. The Mauritanian P. vivax population is shown to be genetically diverse and divergent from populations elsewhere, indicated consistently by genetic distance matrix analysis, principal components analyses, and fixation indices. Only one isolate had a genotype clearly indicating recent importation, from a southeast Asian source. There was no linkage disequilibrium in the local parasite population, and only a small number of infections appeared to be closely genetically related, indicating that there is ongoing genetic recombination consistent with endemic transmission. The P. vivax diversity in a remote mining town was similar to that in the capital Nouakchott, with no indication of local substructure or of epidemic population structure. Drug resistance alleles were virtually absent in Mauritania, in contrast with P. vivax in other areas of the world. Conclusions/Significance The molecular epidemiology indicates that there is long-standing endemic transmission that will be very challenging to eliminate. The virtual absence of drug resistance alleles suggests that most infections have been untreated, and that this endemic infection has been more neglected in comparison to P. vivax elsewhere.


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