The Experts below are selected from a list of 279 Experts worldwide ranked by ideXlab platform
Akira Shinohara - One of the best experts on this subject based on the ideXlab platform.
-
Meiotic Prophase-like pathway for cleavage-independent removal of cohesin for chromosome morphogenesis
Current Genetics, 2019Co-Authors: Kiran Challa, Miki Shinohara, Akira ShinoharaAbstract:Sister chromatid cohesion is essential for chromosome segregation both in mitosis and meiosis. Cohesion between two chromatids is mediated by a protein complex called cohesin. The loading and unloading of the cohesin are tightly regulated during the cell cycle. In vertebrate cells, cohesin is released from chromosomes by two distinct pathways. The best characterized pathway occurs at the onset of anaphase, when the kleisin component of the cohesin is destroyed by a protease, separase. The cleavage of the cohesin by separase releases entrapped sister chromatids allowing anaphase to commence. In addition, prior to the metaphase–anaphase transition, most of cohesin is removed from chromosomes in a cleavage-independent manner. This cohesin release is referred to as the Prophase pathway. In meiotic cells, sister chromatid cohesion is essential for the segregation of homologous chromosomes during meiosis I. Thus, it was assumed that the Prophase pathway for cohesin removal from chromosome arms would be suppressed during meiosis to avoid errors in chromosome segregation. However, recent studies revealed the presence of a meiosis-specific Prophase-like pathway for cleavage-independent removal of cohesin during late Prophase I in different organisms. In budding yeast, the cleavage-independent removal of cohesin is mediated through meiosis-specific phosphorylation of cohesin subunits, Rec8, the meiosis-specific kleisin, and the yeast Wapl ortholog, Rad61/Wpl1. This pathway plays a role in chromosome morphogenesis during late Prophase I, promoting chromosome compaction. In this review, we give an overview of the Prophase pathway for cohesin dynamics during meiosis, which has a complex regulation leading to differentially localized populations of cohesin along meiotic chromosomes.
-
meiosis specific Prophase like pathway controls cleavage independent release of cohesin by wapl phosphorylation
PLOS Genetics, 2019Co-Authors: Kiran Challa, Miki Shinohara, Ghanim Fajish, Franz Klein, Susan M Gasser, Akira ShinoharaAbstract:Sister chromatid cohesion on chromosome arms is essential for the segregation of homologous chromosomes during meiosis I while it is dispensable for sister chromatid separation during mitosis. It was assumed that, unlike the situation in mitosis, chromosome arms retain cohesion prior to onset of anaphase-I. Paradoxically, reduced immunostaining signals of meiosis-specific cohesin, including the kleisin Rec8, were observed on chromosomes during late Prophase-I of budding yeast. This decrease is seen in the absence of Rec8 cleavage and depends on condensin-mediated recruitment of Polo-like kinase (PLK/Cdc5). In this study, we confirmed that this release indeed accompanies the dissociation of acetylated Smc3 as well as Rec8 from meiotic chromosomes during late Prophase-I. This release requires, in addition to PLK, the cohesin regulator, Wapl (Rad61/Wpl1 in yeast), and Dbf4-dependent Cdc7 kinase (DDK). Meiosis-specific phosphorylation of Rad61/Wpl1 and Rec8 by PLK and DDK collaboratively promote this release. This process is similar to the vertebrate “Prophase” pathway for cohesin release during G2 phase and pro-metaphase. In yeast, meiotic cohesin release coincides with PLK-dependent compaction of chromosomes in late meiotic Prophase-I. We suggest that yeast uses this highly regulated cleavage-independent pathway to remove cohesin during late Prophase-I to facilitate morphogenesis of condensed metaphase-I chromosomes.
-
meiosis specific Prophase like pathway controls cleavage independent release of cohesin by wapl phosphorylation
bioRxiv, 2018Co-Authors: Kiran Challa, Miki Shinohara, Ghanim Fajish, Franz Klein, Susan M Gasser, Akira ShinoharaAbstract:Abstract Sister chromatid cohesion on chromosome arms is essential for the segregation of homologous chromosomes during meiosis I while it is dispensable for sister chromatid separation during mitosis. It was assumed that, unlike the situation in mitosis, chromosome arms retain cohesion prior to onset of anaphase-I. Paradoxically, reduced immunostaining signals of meiosis-specific cohesin, including the kleisin Rec8, from the chromosomes were observed during late Prophase-I of budding yeast. This decrease is seen in the absence of Rec8 cleavage and depends on condensin-mediated recruitment of Polo-like kinase (PLK/Cdc5). In this study, we confirmed that this release indeed accompanies the dissociation of acetylated Smc3 as well as Rec8 from meiotic chromosomes during late Prophase-I. This release requires, in addition to PLK, the cohesin regulator, Wapl (Rad61/Wpl1 in yeast), and Dbf4-dependent Cdc7 kinase (DDK). Meiosis-specific phosphorylation of Rad61/Wpl1 and Rec8 by PLK and DDK collaboratively promote this release. This process is similar to the vertebrate “Prophase” pathway for cohesin release during G2 phase and pro-metaphase. In yeast, meiotic cohesin release coincides with PLK-dependent compaction of chromosomes in late meiotic Prophase-I. We suggest that yeast uses this highly regulated cleavage-independent pathway to remove cohesin during late Prophase-I to facilitate morphogenesis of condensed metaphase-I chromosomes. Author Summary In meiosis the life and health of future generations is decided upon. Any failure in chromosome segregation has a detrimental impact. Therefore, it is currently believed that the physical connections between homologous chromosomes are maintained by meiotic cohesin with exceptional stability. Indeed, it was shown that cohesive cohesin does not show an appreciable turnover during long periods in oocyte development. In this context, it was long assumed but not properly investigated, that the Prophase pathway for cohesin release would be specific to mitotic cells and will be safely suppressed during meiosis so as not to endanger the valuable chromosome connections. However, a previous study on budding yeast meiosis suggests the presence of cleavage-independent pathway of cohesin release during late Prophase-I. In the work presented here we confirmed that the Prophase pathway is not suppressed during meiosis, at least in budding yeast and showed that this cleavage-independent release is regulated by meiosis-specific phosphorylation of two cohesin subunits, Rec8 and Rad61(Wapl) by two cell-cycle regulators, PLK and DDK. Our results suggest that late meiotic Prophase-I actively controls cohesin dynamics on meiotic chromosomes for chromosome segregation.
-
meiosis specific Prophase like pathway controls cleavage independent release of cohesin by wapl
bioRxiv, 2018Co-Authors: Kiran Challa, Miki Shinohara, Ghanim Fajish, Franz Klein, Susan M Gasser, Akira ShinoharaAbstract:Summary Sister chromatid cohesion on chromosome arms is essential for the segregation of homologous chromosomes during meiosis I while it is dispensable for sister chromatid separation during mitosis. It was assumed that, unlike the situation in mitosis, chromosome arms retain cohesion prior to onset of anaphase-I. Here we show that approximately half of the meiosis-specific cohesin, including the kleisin Rec8, is released from meiotic chromosomes during late Prophase-I. This release is independent of cleavage by separase and requires the cohesin regulator, Wapl (Rad61/Wpl1 in yeast), and Polo-like kinase (PLK). Meiosis-specific phosphorylation of Rad61/Wpl1 and Rec8 by PLK and the Dbf4-dependent Cdc7 kinase (DDK) promote this release. This process is similar to the vertebrate “Prophase” pathway for cohesin release during G2 phase and pro-metaphase. In yeast, meiotic cohesin release coincides with PLK-dependent compaction of chromosomes in late meiotic Prophase-I. We suggest that yeast uses this highly regulated cleavage-independent pathway to remove cohesin during late Prophase-I in order to facilitate chromosome morphogenesis.
-
rapid telomere movement in meiotic Prophase is promoted by ndj1 mps3 and csm4 and is modulated by recombination
Cell, 2008Co-Authors: Michael N Conrad, Miki Shinohara, Akira Shinohara, Chihying Lee, Gene Chao, Hiromichi Kosaka, Joseangel Conchello, Michael E DresserAbstract:Summary Haploidization of the genome in meiosis requires that chromosomes be sorted exclusively into pairs stabilized by synaptonemal complexes (SCs) and crossovers. This sorting and pairing is accompanied by active chromosome positioning in meiotic Prophase in which telomeres cluster near the spindle pole to form the bouquet before dispersing around the nuclear envelope. We now describe telomere-led rapid Prophase movements (RPMs) that frequently exceed 1 μm/s and persist throughout meiotic Prophase. Bouquet formation and RPMs depend on NDJ1 , MPS3 , and a new member of this pathway, CSM4 , which encodes a meiosis-specific nuclear envelope protein required specifically for telomere mobility. RPMs initiate independently of recombination but differ quantitatively in mutants that fail to complete recombination, suggesting that RPMs respond to recombination status. Together with recombination defects described for ndj1 , our observations suggest that RPMs and SCs balance the disruption and stabilization of recombinational interactions, respectively, to regulate crossing over.
Kiran Challa - One of the best experts on this subject based on the ideXlab platform.
-
Meiotic Prophase-like pathway for cleavage-independent removal of cohesin for chromosome morphogenesis
Current Genetics, 2019Co-Authors: Kiran Challa, Miki Shinohara, Akira ShinoharaAbstract:Sister chromatid cohesion is essential for chromosome segregation both in mitosis and meiosis. Cohesion between two chromatids is mediated by a protein complex called cohesin. The loading and unloading of the cohesin are tightly regulated during the cell cycle. In vertebrate cells, cohesin is released from chromosomes by two distinct pathways. The best characterized pathway occurs at the onset of anaphase, when the kleisin component of the cohesin is destroyed by a protease, separase. The cleavage of the cohesin by separase releases entrapped sister chromatids allowing anaphase to commence. In addition, prior to the metaphase–anaphase transition, most of cohesin is removed from chromosomes in a cleavage-independent manner. This cohesin release is referred to as the Prophase pathway. In meiotic cells, sister chromatid cohesion is essential for the segregation of homologous chromosomes during meiosis I. Thus, it was assumed that the Prophase pathway for cohesin removal from chromosome arms would be suppressed during meiosis to avoid errors in chromosome segregation. However, recent studies revealed the presence of a meiosis-specific Prophase-like pathway for cleavage-independent removal of cohesin during late Prophase I in different organisms. In budding yeast, the cleavage-independent removal of cohesin is mediated through meiosis-specific phosphorylation of cohesin subunits, Rec8, the meiosis-specific kleisin, and the yeast Wapl ortholog, Rad61/Wpl1. This pathway plays a role in chromosome morphogenesis during late Prophase I, promoting chromosome compaction. In this review, we give an overview of the Prophase pathway for cohesin dynamics during meiosis, which has a complex regulation leading to differentially localized populations of cohesin along meiotic chromosomes.
-
meiosis specific Prophase like pathway controls cleavage independent release of cohesin by wapl phosphorylation
PLOS Genetics, 2019Co-Authors: Kiran Challa, Miki Shinohara, Ghanim Fajish, Franz Klein, Susan M Gasser, Akira ShinoharaAbstract:Sister chromatid cohesion on chromosome arms is essential for the segregation of homologous chromosomes during meiosis I while it is dispensable for sister chromatid separation during mitosis. It was assumed that, unlike the situation in mitosis, chromosome arms retain cohesion prior to onset of anaphase-I. Paradoxically, reduced immunostaining signals of meiosis-specific cohesin, including the kleisin Rec8, were observed on chromosomes during late Prophase-I of budding yeast. This decrease is seen in the absence of Rec8 cleavage and depends on condensin-mediated recruitment of Polo-like kinase (PLK/Cdc5). In this study, we confirmed that this release indeed accompanies the dissociation of acetylated Smc3 as well as Rec8 from meiotic chromosomes during late Prophase-I. This release requires, in addition to PLK, the cohesin regulator, Wapl (Rad61/Wpl1 in yeast), and Dbf4-dependent Cdc7 kinase (DDK). Meiosis-specific phosphorylation of Rad61/Wpl1 and Rec8 by PLK and DDK collaboratively promote this release. This process is similar to the vertebrate “Prophase” pathway for cohesin release during G2 phase and pro-metaphase. In yeast, meiotic cohesin release coincides with PLK-dependent compaction of chromosomes in late meiotic Prophase-I. We suggest that yeast uses this highly regulated cleavage-independent pathway to remove cohesin during late Prophase-I to facilitate morphogenesis of condensed metaphase-I chromosomes.
-
meiosis specific Prophase like pathway controls cleavage independent release of cohesin by wapl phosphorylation
bioRxiv, 2018Co-Authors: Kiran Challa, Miki Shinohara, Ghanim Fajish, Franz Klein, Susan M Gasser, Akira ShinoharaAbstract:Abstract Sister chromatid cohesion on chromosome arms is essential for the segregation of homologous chromosomes during meiosis I while it is dispensable for sister chromatid separation during mitosis. It was assumed that, unlike the situation in mitosis, chromosome arms retain cohesion prior to onset of anaphase-I. Paradoxically, reduced immunostaining signals of meiosis-specific cohesin, including the kleisin Rec8, from the chromosomes were observed during late Prophase-I of budding yeast. This decrease is seen in the absence of Rec8 cleavage and depends on condensin-mediated recruitment of Polo-like kinase (PLK/Cdc5). In this study, we confirmed that this release indeed accompanies the dissociation of acetylated Smc3 as well as Rec8 from meiotic chromosomes during late Prophase-I. This release requires, in addition to PLK, the cohesin regulator, Wapl (Rad61/Wpl1 in yeast), and Dbf4-dependent Cdc7 kinase (DDK). Meiosis-specific phosphorylation of Rad61/Wpl1 and Rec8 by PLK and DDK collaboratively promote this release. This process is similar to the vertebrate “Prophase” pathway for cohesin release during G2 phase and pro-metaphase. In yeast, meiotic cohesin release coincides with PLK-dependent compaction of chromosomes in late meiotic Prophase-I. We suggest that yeast uses this highly regulated cleavage-independent pathway to remove cohesin during late Prophase-I to facilitate morphogenesis of condensed metaphase-I chromosomes. Author Summary In meiosis the life and health of future generations is decided upon. Any failure in chromosome segregation has a detrimental impact. Therefore, it is currently believed that the physical connections between homologous chromosomes are maintained by meiotic cohesin with exceptional stability. Indeed, it was shown that cohesive cohesin does not show an appreciable turnover during long periods in oocyte development. In this context, it was long assumed but not properly investigated, that the Prophase pathway for cohesin release would be specific to mitotic cells and will be safely suppressed during meiosis so as not to endanger the valuable chromosome connections. However, a previous study on budding yeast meiosis suggests the presence of cleavage-independent pathway of cohesin release during late Prophase-I. In the work presented here we confirmed that the Prophase pathway is not suppressed during meiosis, at least in budding yeast and showed that this cleavage-independent release is regulated by meiosis-specific phosphorylation of two cohesin subunits, Rec8 and Rad61(Wapl) by two cell-cycle regulators, PLK and DDK. Our results suggest that late meiotic Prophase-I actively controls cohesin dynamics on meiotic chromosomes for chromosome segregation.
-
meiosis specific Prophase like pathway controls cleavage independent release of cohesin by wapl
bioRxiv, 2018Co-Authors: Kiran Challa, Miki Shinohara, Ghanim Fajish, Franz Klein, Susan M Gasser, Akira ShinoharaAbstract:Summary Sister chromatid cohesion on chromosome arms is essential for the segregation of homologous chromosomes during meiosis I while it is dispensable for sister chromatid separation during mitosis. It was assumed that, unlike the situation in mitosis, chromosome arms retain cohesion prior to onset of anaphase-I. Here we show that approximately half of the meiosis-specific cohesin, including the kleisin Rec8, is released from meiotic chromosomes during late Prophase-I. This release is independent of cleavage by separase and requires the cohesin regulator, Wapl (Rad61/Wpl1 in yeast), and Polo-like kinase (PLK). Meiosis-specific phosphorylation of Rad61/Wpl1 and Rec8 by PLK and the Dbf4-dependent Cdc7 kinase (DDK) promote this release. This process is similar to the vertebrate “Prophase” pathway for cohesin release during G2 phase and pro-metaphase. In yeast, meiotic cohesin release coincides with PLK-dependent compaction of chromosomes in late meiotic Prophase-I. We suggest that yeast uses this highly regulated cleavage-independent pathway to remove cohesin during late Prophase-I in order to facilitate chromosome morphogenesis.
Jan Motlik - One of the best experts on this subject based on the ideXlab platform.
-
Prophase i arrest and progression to metaphase i in mouse oocytes comparison of resumption of meiosis and recovery from g2 arrest in somatic cells
Molecular Human Reproduction, 2010Co-Authors: Petr Solc, Richard M. Schultz, Jan MotlikAbstract:Mammalian oocytes are arrested at Prophase I until puberty when luteinizing hormone (LH) induces resumption of meiosis of follicle-enclosed oocytes. Resumption of meiosis is tightly coupled with regulating cyclin-dependent kinase 1 (CDK1) activity. Prophase I arrest depends on inhibitory phosphorylation of CDK1 and anaphase-promoting complex—(APC -CDH1)-mediated regulation of cyclin B levels. Prophase I arrest is maintained by endogenously produced cyclic adenosine monophosphate (cAMP), which activates protein kinase A (PKA) that in turn phosphorylates (and activates) the nuclear kinase WEE2. In addition, PKA-mediated phosphorylation of the phos- phatase CDC25B results in its cytoplasmic retention. The combined effect maintains low levels of CDK1 activity that are not sufficient to initiate resumption of meiosis. LH triggers synthesis of epidermal growth factor-like factors in mural granulosa cells and leads to reduced cGMP transfer from cumulus cells to oocytes via gap junctions that couple the two cell types. cGMP inhibits oocyte phosphodiesterase 3A (PDE3A) and a decline in oocyte cGMP results in increased PDE3A activity. The ensuing decrease in oocyte cAMP triggers maturation by alleviating the aforementioned phosphorylations of WEE2 and CDC25B. As a direct consequence CDC25B translocates into the nucleus. The resulting activation of CDK1 also promotes extrusion of WEE2 from the nucleus thereby providing a positive amplification mechanism for CDK1 activation. Other kinases, e.g. protein kinase B, Aurora kinase A and polo-like kinase 1, also participate in resumption of meiosis. Mechanisms governing meiotic Prophase I arrest and resumption of meiosis share common features with DNA damage-induced mitotic G2- checkpoint arrest and checkpoint recovery, respectively. These common features include CDC14B-dependent activation of APC -CDH1 in Prophase I arrested oocytes or G2-arrested somatic cells, and CDC25B-dependent cell cycle resumption in both oocytes and somatic cells.
Miki Shinohara - One of the best experts on this subject based on the ideXlab platform.
-
Meiotic Prophase-like pathway for cleavage-independent removal of cohesin for chromosome morphogenesis
Current Genetics, 2019Co-Authors: Kiran Challa, Miki Shinohara, Akira ShinoharaAbstract:Sister chromatid cohesion is essential for chromosome segregation both in mitosis and meiosis. Cohesion between two chromatids is mediated by a protein complex called cohesin. The loading and unloading of the cohesin are tightly regulated during the cell cycle. In vertebrate cells, cohesin is released from chromosomes by two distinct pathways. The best characterized pathway occurs at the onset of anaphase, when the kleisin component of the cohesin is destroyed by a protease, separase. The cleavage of the cohesin by separase releases entrapped sister chromatids allowing anaphase to commence. In addition, prior to the metaphase–anaphase transition, most of cohesin is removed from chromosomes in a cleavage-independent manner. This cohesin release is referred to as the Prophase pathway. In meiotic cells, sister chromatid cohesion is essential for the segregation of homologous chromosomes during meiosis I. Thus, it was assumed that the Prophase pathway for cohesin removal from chromosome arms would be suppressed during meiosis to avoid errors in chromosome segregation. However, recent studies revealed the presence of a meiosis-specific Prophase-like pathway for cleavage-independent removal of cohesin during late Prophase I in different organisms. In budding yeast, the cleavage-independent removal of cohesin is mediated through meiosis-specific phosphorylation of cohesin subunits, Rec8, the meiosis-specific kleisin, and the yeast Wapl ortholog, Rad61/Wpl1. This pathway plays a role in chromosome morphogenesis during late Prophase I, promoting chromosome compaction. In this review, we give an overview of the Prophase pathway for cohesin dynamics during meiosis, which has a complex regulation leading to differentially localized populations of cohesin along meiotic chromosomes.
-
meiosis specific Prophase like pathway controls cleavage independent release of cohesin by wapl phosphorylation
PLOS Genetics, 2019Co-Authors: Kiran Challa, Miki Shinohara, Ghanim Fajish, Franz Klein, Susan M Gasser, Akira ShinoharaAbstract:Sister chromatid cohesion on chromosome arms is essential for the segregation of homologous chromosomes during meiosis I while it is dispensable for sister chromatid separation during mitosis. It was assumed that, unlike the situation in mitosis, chromosome arms retain cohesion prior to onset of anaphase-I. Paradoxically, reduced immunostaining signals of meiosis-specific cohesin, including the kleisin Rec8, were observed on chromosomes during late Prophase-I of budding yeast. This decrease is seen in the absence of Rec8 cleavage and depends on condensin-mediated recruitment of Polo-like kinase (PLK/Cdc5). In this study, we confirmed that this release indeed accompanies the dissociation of acetylated Smc3 as well as Rec8 from meiotic chromosomes during late Prophase-I. This release requires, in addition to PLK, the cohesin regulator, Wapl (Rad61/Wpl1 in yeast), and Dbf4-dependent Cdc7 kinase (DDK). Meiosis-specific phosphorylation of Rad61/Wpl1 and Rec8 by PLK and DDK collaboratively promote this release. This process is similar to the vertebrate “Prophase” pathway for cohesin release during G2 phase and pro-metaphase. In yeast, meiotic cohesin release coincides with PLK-dependent compaction of chromosomes in late meiotic Prophase-I. We suggest that yeast uses this highly regulated cleavage-independent pathway to remove cohesin during late Prophase-I to facilitate morphogenesis of condensed metaphase-I chromosomes.
-
meiosis specific Prophase like pathway controls cleavage independent release of cohesin by wapl phosphorylation
bioRxiv, 2018Co-Authors: Kiran Challa, Miki Shinohara, Ghanim Fajish, Franz Klein, Susan M Gasser, Akira ShinoharaAbstract:Abstract Sister chromatid cohesion on chromosome arms is essential for the segregation of homologous chromosomes during meiosis I while it is dispensable for sister chromatid separation during mitosis. It was assumed that, unlike the situation in mitosis, chromosome arms retain cohesion prior to onset of anaphase-I. Paradoxically, reduced immunostaining signals of meiosis-specific cohesin, including the kleisin Rec8, from the chromosomes were observed during late Prophase-I of budding yeast. This decrease is seen in the absence of Rec8 cleavage and depends on condensin-mediated recruitment of Polo-like kinase (PLK/Cdc5). In this study, we confirmed that this release indeed accompanies the dissociation of acetylated Smc3 as well as Rec8 from meiotic chromosomes during late Prophase-I. This release requires, in addition to PLK, the cohesin regulator, Wapl (Rad61/Wpl1 in yeast), and Dbf4-dependent Cdc7 kinase (DDK). Meiosis-specific phosphorylation of Rad61/Wpl1 and Rec8 by PLK and DDK collaboratively promote this release. This process is similar to the vertebrate “Prophase” pathway for cohesin release during G2 phase and pro-metaphase. In yeast, meiotic cohesin release coincides with PLK-dependent compaction of chromosomes in late meiotic Prophase-I. We suggest that yeast uses this highly regulated cleavage-independent pathway to remove cohesin during late Prophase-I to facilitate morphogenesis of condensed metaphase-I chromosomes. Author Summary In meiosis the life and health of future generations is decided upon. Any failure in chromosome segregation has a detrimental impact. Therefore, it is currently believed that the physical connections between homologous chromosomes are maintained by meiotic cohesin with exceptional stability. Indeed, it was shown that cohesive cohesin does not show an appreciable turnover during long periods in oocyte development. In this context, it was long assumed but not properly investigated, that the Prophase pathway for cohesin release would be specific to mitotic cells and will be safely suppressed during meiosis so as not to endanger the valuable chromosome connections. However, a previous study on budding yeast meiosis suggests the presence of cleavage-independent pathway of cohesin release during late Prophase-I. In the work presented here we confirmed that the Prophase pathway is not suppressed during meiosis, at least in budding yeast and showed that this cleavage-independent release is regulated by meiosis-specific phosphorylation of two cohesin subunits, Rec8 and Rad61(Wapl) by two cell-cycle regulators, PLK and DDK. Our results suggest that late meiotic Prophase-I actively controls cohesin dynamics on meiotic chromosomes for chromosome segregation.
-
meiosis specific Prophase like pathway controls cleavage independent release of cohesin by wapl
bioRxiv, 2018Co-Authors: Kiran Challa, Miki Shinohara, Ghanim Fajish, Franz Klein, Susan M Gasser, Akira ShinoharaAbstract:Summary Sister chromatid cohesion on chromosome arms is essential for the segregation of homologous chromosomes during meiosis I while it is dispensable for sister chromatid separation during mitosis. It was assumed that, unlike the situation in mitosis, chromosome arms retain cohesion prior to onset of anaphase-I. Here we show that approximately half of the meiosis-specific cohesin, including the kleisin Rec8, is released from meiotic chromosomes during late Prophase-I. This release is independent of cleavage by separase and requires the cohesin regulator, Wapl (Rad61/Wpl1 in yeast), and Polo-like kinase (PLK). Meiosis-specific phosphorylation of Rad61/Wpl1 and Rec8 by PLK and the Dbf4-dependent Cdc7 kinase (DDK) promote this release. This process is similar to the vertebrate “Prophase” pathway for cohesin release during G2 phase and pro-metaphase. In yeast, meiotic cohesin release coincides with PLK-dependent compaction of chromosomes in late meiotic Prophase-I. We suggest that yeast uses this highly regulated cleavage-independent pathway to remove cohesin during late Prophase-I in order to facilitate chromosome morphogenesis.
-
rapid telomere movement in meiotic Prophase is promoted by ndj1 mps3 and csm4 and is modulated by recombination
Cell, 2008Co-Authors: Michael N Conrad, Miki Shinohara, Akira Shinohara, Chihying Lee, Gene Chao, Hiromichi Kosaka, Joseangel Conchello, Michael E DresserAbstract:Summary Haploidization of the genome in meiosis requires that chromosomes be sorted exclusively into pairs stabilized by synaptonemal complexes (SCs) and crossovers. This sorting and pairing is accompanied by active chromosome positioning in meiotic Prophase in which telomeres cluster near the spindle pole to form the bouquet before dispersing around the nuclear envelope. We now describe telomere-led rapid Prophase movements (RPMs) that frequently exceed 1 μm/s and persist throughout meiotic Prophase. Bouquet formation and RPMs depend on NDJ1 , MPS3 , and a new member of this pathway, CSM4 , which encodes a meiosis-specific nuclear envelope protein required specifically for telomere mobility. RPMs initiate independently of recombination but differ quantitatively in mutants that fail to complete recombination, suggesting that RPMs respond to recombination status. Together with recombination defects described for ndj1 , our observations suggest that RPMs and SCs balance the disruption and stabilization of recombinational interactions, respectively, to regulate crossing over.
Daniel R Cameriniotero - One of the best experts on this subject based on the ideXlab platform.
-
the expression profile of the major mouse spo11 isoforms indicates that spo11β introduces double strand breaks and suggests that spo11α has an additional role in Prophase in both spermatocytes and oocytes
Molecular and Cellular Biology, 2010Co-Authors: Marina A Bellani, Kingsley A Boateng, Dianne Mcleod, Daniel R CamerinioteroAbstract:Both in mice and humans, two major SPO11 isoforms are generated by alternative splicing: SPO11α (exon 2 skipped) and SPO11β. Thus, the alternative splicing event must have emerged before the mouse and human lineages diverged and was maintained during 90 million years of evolution, arguing for an essential role for both isoforms. Here we demonstrate that developmental regulation of alternative splicing at the Spo11 locus governs the sequential expression of SPO11 isoforms in male meiotic Prophase. Protein quantification in juvenile mice and in Prophase mutants indicates that early spermatocytes synthesize primarily SPO11β. Estimation of the number of SPO11 dimers (ββ/αβ/αα) in mutants in which spermatocytes undergo a normal number of double strand breaks but arrest in midProphase due to inefficient repair argues for a role for SPO11β-containing dimers in introducing the breaks in leptonema. Expression kinetics in males suggested a role for SPO11α in pachytene/diplotene spermatocytes. Nevertheless, we found that both alternative transcripts can be detected in oocytes throughout Prophase I, arguing against a male-specific function for this isoform. Altogether, our data support a role for SPO11α in mid- to late Prophase, presumably acting as a topoisomerase, that would be conserved in male and female meiocytes.
