scholarly journals TOP-2 is differentially required for the proper maintenance of cohesin on meiotic chromosomes in C. elegans spermatogenesis and oogenesis

2021 ◽  
Author(s):  
Aimee Jaramillo-Lambert ◽  
Christine Kiely Rourke
Keyword(s):  
Sister Chromatid ◽  
Topoisomerase Ii ◽  
Meiotic Chromosome ◽  
Sister Chromatid Cohesion ◽  
Chromosome Length ◽  
Aurora B ◽  
Loss Of Function ◽  
Late Prophase ◽  
Prophase I ◽  
Chromatid Cohesion

During meiotic prophase I, accurate segregation of homologous chromosomes requires the establishment of a chromosomes with a meiosis-specific architecture. Sister chromatid cohesins and the enzyme Topoisomerase II are important components of meiotic chromosome axes, but the relationship of these proteins in the context of meiotic chromosome segregation is poorly defined. Here, we analyzed the role of Topoisomerase II (TOP-2) in the timely release of sister chromatid cohesins during spermatogenesis and oogenesis of Caenorhabditis elegans. We show that there is a different requirement for TOP-2 in meiosis of spermatogenesis and oogenesis. The loss-of-function mutation top-2(it7) results in premature REC-8 removal in spermatogenesis, but not oogenesis. This is due to a failure to maintain the HORMA-domain proteins HTP-1 and HTP-2 (HTP-1/2) on chromosome axes at diakinesis and mislocalization of the downstream components that control sister chromatid cohesion release including Aurora B kinase. In oogenesis, top-2(it7) causes a delay in the localization of Aurora B to oocyte chromosomes but can be rescued through premature activation of the maturation promoting factor via knock-down of the inhibitor kinase WEE-1.3. The delay in Aurora B localization is associated with an increase in the length of diakinesis chromosomes and wee-1.3 RNAi mediated rescue of Auorora B localization in top-2(it7) is associated with a decrease in chromosome length. Our results imply that the sex-specific effects of Topoisomerase II on sister chromatid cohesion release are due to differences in the temporal regulation of meiosis and chromosome structure in late prophase I in spermatogenesis and oogenesis.

scholarly journals Shugoshin is essential for meiotic prophase checkpoints in C. elegans

2018 ◽  
Author(s):  
Tisha Bohr ◽  
Christian R. Nelson ◽  
Stefani Giacopazzi ◽  
Piero Lamelza ◽  
Needhi Bhalla
Keyword(s):  
Sister Chromatid ◽  
Meiotic Prophase ◽  
Meiotic Chromosome ◽  
Sister Chromatid Cohesion ◽  
Chromosomal Protein ◽  
Loss Of Function ◽  
Chromosome Architecture ◽  
C Elegans ◽  
Meiotic Chromosomes ◽  
Chromatid Cohesion

AbstractThe conserved factor Shugoshin is dispensable in C. elegans for the two-step loss of sister chromatid cohesion that directs the proper segregation of meiotic chromosomes. We show that the C. elegans ortholog of Shugoshin, SGO-1, is required for checkpoint activity in meiotic prophase. This role in checkpoint function is similar to that of the meiotic chromosomal protein, HTP-3. Null sgo-1 mutants exhibit additional phenotypes similar to that of a partial loss of function allele of HTP-3: premature synaptonemal complex disassembly, the activation of alternate DNA repair pathways and an inability to recruit a conserved effector of the DNA damage pathway, HUS-1. SGO-1 localizes to pre-meiotic nuclei, when HTP-3 is present but not yet loaded onto chromosome axes, suggesting an early role in regulating meiotic chromosome metabolism. We propose that SGO-1 acts during pre-meiotic replication to ensure fully functional meiotic chromosome architecture, rendering these chromosomes competent for checkpoint activity and normal progression of meiotic recombination. Given that most research on Shugoshin has been focused on its regulation of sister chromatid cohesion in meiosis, this novel role may be conserved but previously uncharacterized in other organisms. Further, our findings expand the repertoire of Shugoshin’s functions beyond coordinating regulatory activities at the centromere.

scholarly journals Double or nothing: a Drosophila mutation affecting meiotic chromosome segregation in both females and males.

Genetics ◽  
1994 ◽  
Vol 136 (3) ◽  
pp. 953-964 ◽  
Author(s):  
D P Moore ◽  
W Y Miyazaki ◽  
J E Tomkiel ◽  
T L Orr-Weaver
Keyword(s):  
Cell Death ◽  
Chromosome Segregation ◽  
Sister Chromatid ◽  
Meiotic Chromosome ◽  
Sister Chromatid Cohesion ◽  
Aberrant Chromosome ◽  
Chromatid Cohesion ◽  
Meiotic Nondisjunction ◽  
Lethal Allele ◽  
Meiosis I

Abstract We describe a Drosophila mutation, Double or nothing (Dub), that causes meiotic nondisjunction in a conditional, dominant manner. Previously isolated mutations in Drosophila specifically affect meiosis either in females or males, with the exception of the mei-S332 and ord genes which are required for proper sister-chromatid cohesion. Dub is unusual in that it causes aberrant chromosome segregation almost exclusively in meiosis I in both sexes. In Dub mutant females both nonexchange and exchange chromosomes undergo nondisjunction, but the effect of Dub on nonexchange chromosomes is more pronounced. Dub reduces recombination levels slightly. Multiple nondisjoined chromosomes frequently cosegregate to the same pole. Dub results in nondisjunction of all chromosomes in meiosis I of males, although the levels are lower than in females. When homozygous, Dub is a conditional lethal allele and exhibits phenotypes consistent with cell death.

scholarly journals Crossovers trigger a remodeling of meiotic chromosome axis composition that is linked to two-step loss of sister chromatid cohesion

2008 ◽  
Vol 22 (20) ◽  
pp. 2886-2901 ◽  
Author(s):  
E. Martinez-Perez ◽  
M. Schvarzstein ◽  
C. Barroso ◽  
J. Lightfoot ◽  
A. F. Dernburg ◽  
...  
Keyword(s):  
Sister Chromatid ◽  
Meiotic Chromosome ◽  
Sister Chromatid Cohesion ◽  
Chromatid Cohesion ◽  
Chromosome Axis

scholarly journals INCENP and Aurora B Promote Meiotic Sister Chromatid Cohesion through Localization of the Shugoshin MEI-S332 in Drosophila

2006 ◽  
Vol 11 (1) ◽  
pp. 57-68 ◽  
Author(s):  
Tamar D. Resnick ◽  
David L. Satinover ◽  
Fiona MacIsaac ◽  
P. Todd Stukenberg ◽  
William C. Earnshaw ◽  
...  
Keyword(s):  
Sister Chromatid ◽  
Sister Chromatid Cohesion ◽  
Aurora B ◽  
Chromatid Cohesion

scholarly journals The Multiple Roles of Cohesin in Meiotic Chromosome Morphogenesis and Pairing

2009 ◽  
Vol 20 (3) ◽  
pp. 1030-1047 ◽  
Author(s):  
Gloria A. Brar ◽  
Andreas Hochwagen ◽  
Ly-sha S. Ee ◽  
Angelika Amon
Keyword(s):  
Sister Chromatid ◽  
Meiotic Prophase ◽  
Meiotic Chromosome ◽  
Sister Chromatid Cohesion ◽  
Multiple Roles ◽  
Axis Formation ◽  
Chromatid Cohesion ◽  
Cohesin Subunit ◽  
Chromosome Axis ◽  
Segregation Of Chromosomes

Sister chromatid cohesion, mediated by cohesin complexes, is laid down during DNA replication and is essential for the accurate segregation of chromosomes. Previous studies indicated that, in addition to their cohesion function, cohesins are essential for completion of recombination, pairing, meiotic chromosome axis formation, and assembly of the synaptonemal complex (SC). Using mutants in the cohesin subunit Rec8, in which phosphorylated residues were mutated to alanines, we show that cohesin phosphorylation is not only important for cohesin removal, but that cohesin's meiotic prophase functions are distinct from each other. We find pairing and SC formation to be dependent on Rec8, but independent of the presence of a sister chromatid and hence sister chromatid cohesion. We identified mutations in REC8 that differentially affect Rec8's cohesion, pairing, recombination, chromosome axis and SC assembly function. These findings define Rec8 as a key determinant of meiotic chromosome morphogenesis and a central player in multiple meiotic events.

scholarly journals LAB-1 Targets PP1 and Restricts Aurora B Kinase upon Entrance into Meiosis to Promote Sister Chromatid Cohesion

PLoS Biology ◽  
2012 ◽  
Vol 10 (8) ◽  
pp. e1001378 ◽  
Author(s):  
Yonatan B. Tzur ◽  
Carlos Egydio de Carvalho ◽  
Saravanapriah Nadarajan ◽  
Ivo Van Bostelen ◽  
Yanjie Gu ◽  
...  
Keyword(s):  
Sister Chromatid ◽  
Sister Chromatid Cohesion ◽  
Aurora B ◽  
Aurora B Kinase ◽  
Chromatid Cohesion

scholarly journals Tex19.1 inhibits the N-end rule pathway and maintains acetylated SMC3 cohesin and sister chromatid cohesion in oocytes

2020 ◽  
Vol 219 (5) ◽  
Author(s):  
Judith Reichmann ◽  
Karen Dobie ◽  
Lisa M. Lister ◽  
James H. Crichton ◽  
Diana Best ◽  
...  
Keyword(s):  
Down Syndrome ◽  
Protein Degradation ◽  
Sister Chromatid ◽  
Meiotic Chromosome ◽  
Sister Chromatid Cohesion ◽  
Protein Activity ◽  
Mouse Oocytes ◽  
Chromatid Cohesion ◽  
Age Dependent ◽  
Female Germline

Age-dependent oocyte aneuploidy, a major cause of Down syndrome, is associated with declining sister chromatid cohesion in postnatal oocytes. Here we show that cohesion in postnatal mouse oocytes is regulated by Tex19.1. We show Tex19.1−/− oocytes have defects maintaining chiasmata, missegregate their chromosomes during meiosis, and transmit aneuploidies to the next generation. Furthermore, we show that mouse Tex19.1 inhibits N-end rule protein degradation mediated by its interacting partner UBR2, and that Ubr2 itself has a previously undescribed role in negatively regulating the acetylated SMC3 subpopulation of cohesin in mitotic somatic cells. Lastly, we show that acetylated SMC3 is associated with meiotic chromosome axes in mouse oocytes, and that this population of cohesin is specifically depleted in the absence of Tex19.1. These findings indicate that Tex19.1 regulates UBR protein activity to maintain acetylated SMC3 and sister chromatid cohesion in postnatal oocytes and prevent aneuploidy from arising in the female germline.

scholarly journals Pericentromeric Sister Chromatid Cohesion Promotes Kinetochore Biorientation

2009 ◽  
Vol 20 (17) ◽  
pp. 3818-3827 ◽  
Author(s):  
Tessie M. Ng ◽  
William G. Waples ◽  
Brigitte D. Lavoie ◽  
Sue Biggins
Keyword(s):  
Protein Kinase ◽  
Genetic Analysis ◽  
Chromosome Segregation ◽  
Sister Chromatid ◽  
Budding Yeast ◽  
Sister Chromatid Cohesion ◽  
Specific Role ◽  
Aurora B ◽  
Chromatid Cohesion ◽  
Yeast Genes

Accurate chromosome segregation depends on sister kinetochores making bioriented attachments to microtubules from opposite poles. An essential regulator of biorientation is the Ipl1/Aurora B protein kinase that destabilizes improper microtubule–kinetochore attachments. To identify additional biorientation pathways, we performed a systematic genetic analysis between the ipl1-321 allele and all nonessential budding yeast genes. One of the mutants, mcm21Δ, precociously separates pericentromeres and this is associated with a defect in the binding of the Scc2 cohesin-loading factor at the centromere. Strikingly, Mcm21 becomes essential for biorientation when Ipl1 function is reduced, and this appears to be related to its role in pericentromeric cohesion. When pericentromeres are artificially tethered, Mcm21 is no longer needed for biorientation despite decreased Ipl1 activity. Taken together, these data reveal a specific role for pericentromeric linkage in ensuring kinetochore biorientation.

scholarly journals Tex19.1 Regulates Acetylated SMC3 Cohesin and Prevents Aneuploidy in Mouse Oocytes

2017 ◽  
Author(s):  
Judith Reichmann ◽  
Karen Dobie ◽  
Lisa M. Lister ◽  
Diana Best ◽  
James H. Crichton ◽  
...  
Keyword(s):  
Down Syndrome ◽  
Ubiquitin Ligase ◽  
Sister Chromatid ◽  
Meiotic Chromosome ◽  
E3 Ubiquitin Ligase ◽  
Sister Chromatid Cohesion ◽  
Mouse Oocytes ◽  
Chromatid Cohesion ◽  
Age Dependent ◽  
Female Germline

AbstractAge-dependent oocyte aneuploidy, a major cause of Down syndrome, is associated with declining sister chromatid cohesion in postnatal oocytes. Here we show that cohesion in postnatal mouse oocytes is regulated by Tex19.1. We show that Tex19.1-/- oocytes have defects in the maintenance of chiasmata, mis-segregate their chromosomes during meiosis, and transmit aneuploidies to the next generation. By reconstituting aspects of this pathway in mitotic somatic cells, we show that Tex19.1 regulates an acetylated SMC3-marked subpopulation of cohesin by inhibiting the activity of the E3 ubiquitin ligase UBR2 towards specific substrates, and that UBR2 itself has a previously undescribed role in negatively regulating acetylated SMC3. Lastly, we show that acetylated SMC3 is associated with meiotic chromosome axes in oocytes, but that this is reduced in the absence of Tex19.1. These findings indicate that Tex19.1 maintains acetylated SMC3 and sister chromatid cohesion in postnatal oocytes, and prevents aneuploidy in the female germline.

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