sister chromatids
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2022 ◽  
Vol 22 (1) ◽  
Author(s):  
Helal A. Ansari ◽  
Nicholas W. Ellison ◽  
Isabelle M. Verry ◽  
Warren M. Williams

Abstract Background Unreduced gametes, a driving force in the widespread polyploidization and speciation of flowering plants, occur relatively frequently in interspecific or intergeneric hybrids. Studies of the mechanisms leading to 2n gamete formation, mainly in the wheat tribe Triticeae have shown that unreductional meiosis is often associated with chromosome asynapsis during the first meiotic division. The present study explored the mechanisms of meiotic nonreduction leading to functional unreduced gametes in an interspecific Trifolium (clover) hybrid with three sub-genomes from T. ambiguum and one sub-genome from T. occidentale. Results Unreductional meiosis leading to 2n gametes occurred when there was a high frequency of asynapsis during the first meiotic division. In this hybrid, approximately 39% of chromosomes were unpaired at metaphase I. Within the same cell at anaphase I, sister chromatids of univalents underwent precocious separation and formed laggard chromatids whereas paired chromosomes segregated without separation of sister chromatids as in normal meiosis. This asynchrony was frequently accompanied by incomplete or no movement of chromosomes toward the poles and restitution leading to unreduced chromosome constitutions. Reductional meiosis was restored in progeny where asynapsis frequencies were low. Two progeny plants with approximately 5 and 7% of unpaired chromosomes at metaphase I showed full restoration of reductional meiosis. Conclusions The study revealed that formation of 2n gametes occurred when asynapsis (univalent) frequency at meiosis I was high, and that normal gamete production was restored in the next generation when asynapsis frequencies were low. Asynapsis-dependent 2n gamete formation, previously supported by evidence largely from wheat and its relatives and grasshopper, is also applicable to hybrids from the dicotyledonous plant genus Trifolium. The present results align well with those from these widely divergent organisms and strongly suggest common molecular mechanisms involved in unreduced gamete formation.


Agronomy ◽  
2021 ◽  
Vol 11 (12) ◽  
pp. 2574
Author(s):  
Anna Trojak-Goluch ◽  
Magdalena Kawka-Lipińska ◽  
Katarzyna Wielgusz ◽  
Marcin Praczyk

Polyploidisation is an important process in the evolution of many plant species. An additional set of chromosomes can be derived from intraspecific genome duplication (autopolyploidy) or hybridising divergent genomes and chromosome doubling (allopolyploidy). Special forms of polyploidy are autoallopolyploidy and segmental allopolyploidy. Polyploidy arises from two basic processes: spontaneously occurring disturbances of meiotic division and induced by antimitotic agents’ disruption of mitosis. The first involves the induction and fusion of unreduced gametes, resulting in the formation of triploids and tetraploids. The second process uses antimitotics that disrupt cellular microtubules and prevent chromosome’s sister chromatids motion during anaphase. Colchicine, oryzalin, and trifluralin are the most commonly used antimitotics for inducing polyploids in plants. The exposure time and concentration of the antimitotics and the species, cultivar, genotype, and tissue type affect the efficiency of genome duplication. Polyploids are distinguished from diploids by increased cell size and vegetative parts of plants and increased content of secondary metabolites. Genome duplication generates several changes at the epigenetic level resulting in altered gene expression. Polyploidisation is used in plant breeding to overcome the non-viability and infertility of interspecific hybrids, obtain seedless polyploid cultivars and increase resistance/tolerance to biotic and abiotic factors.


Cells ◽  
2021 ◽  
Vol 10 (12) ◽  
pp. 3455
Author(s):  
Janne J.M. van Schie ◽  
Job de Lange

The cohesin complex facilitates faithful chromosome segregation by pairing the sister chromatids after DNA replication until mitosis. In addition, cohesin contributes to proficient and error-free DNA replication. Replisome progression and establishment of sister chromatid cohesion are intimately intertwined processes. Here, we review how the key factors in DNA replication and cohesion establishment cooperate in unperturbed conditions and during DNA replication stress. We discuss the detailed molecular mechanisms of cohesin recruitment and the entrapment of replicated sister chromatids at the replisome, the subsequent stabilization of sister chromatid cohesion via SMC3 acetylation, as well as the role and regulation of cohesin in the response to DNA replication stress.


2021 ◽  
Author(s):  
Masashi Nambu ◽  
Atsuki Kishikawa ◽  
Takatomi Yamada ◽  
Kento Ichikawa ◽  
Yunosuke Kira ◽  
...  

Kinetochores drive chromosome segregation by mediating chromosome interactions with the spindle. In higher eukaryotes, sister kinetochores are separately positioned on opposite sides of sister centromeres during mitosis, but associate with each other during meiosis I. Kinetochore association facilitates the attachment of sister chromatids to the same pole, enabling the segregation of homologous chromosomes toward opposite poles. In the fission yeast, Schizosaccharomyces pombe, Rec8-containing meiotic cohesin is suggested to establish kinetochore associations by mediating cohesion of the centromere cores. However, cohesin-mediated kinetochore associations on intact chromosomes have never been demonstrated directly. Here, we describe a novel method for the direct evaluation of kinetochore associations on intact chromosomes in live S. pombe cells, and demonstrate that sister kinetochores and the centromere cores are positioned separately on mitotic chromosomes but associate with each other on meiosis I chromosomes. Furthermore, we demonstrate that kinetochore association depends on meiotic cohesin and the cohesin regulators, Moa1 and Mrc1, and requires mating-pheromone signaling for its establishment. These results confirm cohesin-mediated kinetochore association and its regulatory mechanisms, along with the usefulness of the developed method for its analysis.


2021 ◽  
Author(s):  
Yasunori Horikoshi ◽  
Hiroki Shima ◽  
Wataru Kobayashi ◽  
Jiying Sun ◽  
Volker J Schmid ◽  
...  

Genome-based functions are inseparable from the dynamic higher-order architecture of the cell nucleus. In this context, the repair of DNA damage is coordinated by precise spatiotemporal controls that target and regulate the repair machinery required to maintain genome integrity. However, the mechanisms that pair damaged DNA with intact template for repair by homologous recombination (HR) without illegitimate recombination remain unclear. This report highlights the intimate relationship between nuclear architecture and HR in mammalian cells. RAD51, the key recombinase of HR, forms spherical foci in S/G2 phases spontaneously. Using super-resolution microscopy, we show that following induction of DNA double-strand breaks RAD51 foci at damaged sites elongate to bridge between intact and damaged sister chromatids; this assembly occurs within bundle-shaped distinctive nuclear zones, requires interactions of RAD51 with various factors, and precedes ATP-dependent events involved the recombination of intact and damaged DNA. We observed a time-dependent transfer of single-stranded DNA overhangs, generated during HR, into such zones. Our observations suggest that RAD51-mediated homologous pairing during HR takes place within the distinctive nuclear zones to execute appropriate recombination.


Genes ◽  
2021 ◽  
Vol 12 (11) ◽  
pp. 1812
Author(s):  
Matan Arbel ◽  
Karan Choudhary ◽  
Ofri Tfilin ◽  
Martin Kupiec

During each cell duplication, the entirety of the genomic DNA in every cell must be accurately and quickly copied. Given the short time available for the chore, the requirement of many proteins, and the daunting amount of DNA present, DNA replication poses a serious challenge to the cell. A high level of coordination between polymerases and other DNA and chromatin-interacting proteins is vital to complete this task. One of the most important proteins for maintaining such coordination is PCNA. PCNA is a multitasking protein that forms a homotrimeric ring that encircles the DNA. It serves as a processivity factor for DNA polymerases and acts as a landing platform for different proteins interacting with DNA and chromatin. Therefore, PCNA is a signaling hub that influences the rate and accuracy of DNA replication, regulates DNA damage repair, controls chromatin formation during the replication, and the proper segregation of the sister chromatids. With so many essential roles, PCNA recruitment and turnover on the chromatin is of utmost importance. Three different, conserved protein complexes are in charge of loading/unloading PCNA onto DNA. Replication factor C (RFC) is the canonical complex in charge of loading PCNA during the S-phase. The Ctf18 and Elg1 (ATAD5 in mammalian) proteins form complexes similar to RFC, with particular functions in the cell’s nucleus. Here we summarize our current knowledge about the roles of these important factors in yeast and mammals.


2021 ◽  
Author(s):  
Elvira Nikalayevich ◽  
Safia El Jailani ◽  
Damien Cladiere ◽  
Yulia Gryaznova ◽  
Celia Fosse ◽  
...  

To generate haploid gametes, cohesin is removed in a stepwise manner from chromosome arms in meiosis I and the centromere region in meiosis II, to segregate chromosomes and sister chromatids, respectively. Meiotic cohesin removal requires cleavage of the meiosis-specific kleisin subunit Rec8 by the protease Separase[1, 2]. In yeast, Rec8 is kept in a non-phosphorylated state by the action of PP2A-B56, which is localised to the centromere region, thereby preventing cohesin removal from this region in meiosis I[3-5]. However, it is unknown whether Rec8 has to be equally phosphorylated for cleavage, and whether centromeric cohesin protection is indeed brought about by dephosphorylation of Rec8 preventing cleavage, in mammalian meiosis. The identity of one or several potential Rec8-specific kinase(s) is also unknown. This is due to technical challenges, as Rec8 is poorly conserved preventing a direct translation of the knowledge gained from model systems such as yeast and C. elegans to mammals, and additionally, there is no turn-over of Rec8 after cohesion establishment, preventing phospho mutant analysis of functional Rec8. To address how Rec8 cleavage is brought about in mammals, we adapted a biosensor for Separase to study Rec8 cleavage in single mouse oocytes by live imaging, and identified phosphorylation sites promoting cleavage. We found that Rec8 cleavage by Separase depends on Aurora B/C kinase activity, and identified a residue promoting cleavage and being phosphorylated in an Aurora B/C kinase-dependent manner. Accordingly, inhibition of Aurora B/C kinase during meiotic maturation impairs endogenous Rec8 phosphorylation and chromosome segregation.


2021 ◽  
Author(s):  
Marc R Gartenberg ◽  
Melinda S Borrie

Cohesin is a central architectural element of chromosome structure that regulates numerous DNA-based events. The complex holds sister chromatids together until anaphase onset and organizes individual chromosomal DNAs into loops. In vitro, cohesin translocates along DNA and extrudes loops in an ATP-dependent fashion. In vivo, cohesin redistributes in response to transcription as if pushed by RNA polymerase. Direct evidence of processive genomic translocation by the complex, however, is lacking. Here, obstacles of increasing size were tethered to DNA in yeast to detect translocation. The obstacles were built from a GFP-lacI core fused to one or more mCherries. Cohesin translocation was initiated from an upstream gene. A chimera with four mCherries blocked cohesin passage in late G1. During M phase, the threshold barrier to passage depended on the state of cohesion: non-cohesive complexes were also blocked by four mCherries whereas cohesive complexes were blocked by only three mCherries. That synthetic barriers alter cohesin redistribution demonstrates that the complex translocates processively on chromatin in vivo. The approach provides a relative measure of the maximum size of the protein chamber(s) that embraces DNA during cohesin translocation. The data indicate that the cohesive embrace is more restrictive than the embrace of non-cohesive complexes.


2021 ◽  
Author(s):  
Rachael E Barton ◽  
Lucia F Massari ◽  
Daniel Robertson ◽  
Adele L Marston

Cohesin organizes the genome by forming intra-chromosomal loops and inter-sister chromatid linkages. During gamete formation by meiosis, chromosomes are reshaped to support crossover recombination and two consecutive rounds of chromosome segregation. Here we show that Eco1 acetyltransferase positions both chromatin loops and sister chromatid cohesion to organize meiotic chromosomes into functional domains in budding yeast. Eco1 acetylates the Smc3 cohesin subunit in meiotic S phase to establish chromatin boundaries, independently of DNA replication. Boundary formation by Eco1 is critical for prophase exit and for the maintenance of cohesion until meiosis II, but is independent of the ability of Eco1 to antagonize the cohesin-release factor, Wpl1. Conversely, prevention of cohesin release by Wpl1 is essential for centromeric cohesion, kinetochore monoorientation and co-segregation of sister chromatids in meiosis I. Our findings establish Eco1 as a key determinant of chromatin boundaries and cohesion positioning, revealing how local chromosome structuring directs genome transmission into gametes.


2021 ◽  
Author(s):  
Owen J. Chen ◽  
Ester Castellsagué ◽  
Mohamed Moustafa-Kamal ◽  
Javad Nadaf ◽  
Barbara Rivera ◽  
...  

SUMMARYCDC20 is a co-activator of the anaphase promoting complex/cyclosome (APC/C) and is essential for mitotic progression. APC/CCDC20 is inhibited by the spindle assembly checkpoint (SAC), which prevents premature separation of sister chromatids and aneuploidy in daughter cells. Although overexpression of CDC20 is common in many cancers, oncogenic mutations have never been identified in humans. Using whole exome sequencing, we identified heterozygous missense CDC20 variants (L151R and N331K) that segregate with cancer in two families. Characterization of these mutants showed they retain APC/C activation activity but show reduced binding to BUBR1, a component of the SAC. Expression of L151R and N331K promoted mitotic slippage in HeLa cells and primary skin fibroblasts derived from carriers. CRISPR/Cas9 was used to generate mice carrying N331K. Homozygous mice carrying N331K were non-viable, however, heterozygotes displayed accelerated oncogenicity in Myc-driven cancers. These findings highlight an unappreciated role for CDC20 variants as tumor promoting genes in humans.


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