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yeast, deletion of PCH2 alleviates the pachytene arrest caused by asynaptic mutants zip1 and zip2 [8]. Although mouse SYCP1 might be a functional equivalent of Zip1p, because Sycp1 mutant spermatocytes arrest at approximately the same point as Trip13 mutants, there would be no opportunity to observe bypass of Sycp1 −/−. Since Zip2p is present at sites of axial associations, even in zip1 mutants, it has been suggested that Zip2p promotes initiation of chromosome synapsis [38]. These observations raise the possibility that in yeast, Pch2p responds to synapsis polymerization rather than initiation. To test this, we performed epistasis analysis with a Rec8 allele (Rec8Mei8, abbreviated as Rec8 −). Meiotic chromosomes of Rec8 mutant spermatocytes undergo apparent homolog pairing and interhomolog synaptic initiation, but are defective in DSB repair and fail to maintain interhomolog synapsis [39,40]. Rather, sister chromatids appear to synapse and are bound by SYCP1 along their axes. Rec8 mutants do not progress to diplonema or metaphase I. Double mutant analysis indicated that Rec8 is epistatic to Trip13. As in the Spo11 and Mei1 experiments, histology of testes deficient for both REC8 and TRIP13 resembled the Rec8 mutant, with no evidence of progression to metaphase I that occurs in Trip13Gt/Gt mice (Figure 3L and 3M). Immunocytological analysis of spread chromosomes showed a failure of homologous chromosome synapsis in both the Rec8 −/− and Rec8 −/− Trip13Gt/Gt spermatocytes, as previously reported for Rec8 mutants (Figure 5D and 5E) [39,40]."}

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{"project":"2_test","denotations":[{"id":"17696610-10319812-85497920","span":{"begin":102,"end":103},"obj":"10319812"},{"id":"17696610-9590170-85497921","span":{"begin":479,"end":481},"obj":"9590170"},{"id":"17696610-15515002-85497922","span":{"begin":902,"end":904},"obj":"15515002"},{"id":"17696610-15935783-85497923","span":{"begin":905,"end":907},"obj":"15935783"},{"id":"17696610-15515002-85497924","span":{"begin":1560,"end":1562},"obj":"15515002"},{"id":"17696610-15935783-85497925","span":{"begin":1563,"end":1565},"obj":"15935783"},{"id":"T42650","span":{"begin":102,"end":103},"obj":"10319812"},{"id":"T75874","span":{"begin":479,"end":481},"obj":"9590170"},{"id":"T52656","span":{"begin":902,"end":904},"obj":"15515002"},{"id":"T5593","span":{"begin":905,"end":907},"obj":"15935783"},{"id":"T19680","span":{"begin":1560,"end":1562},"obj":"15515002"},{"id":"T88762","span":{"begin":1563,"end":1565},"obj":"15935783"}],"text":"In yeast, deletion of PCH2 alleviates the pachytene arrest caused by asynaptic mutants zip1 and zip2 [8]. Although mouse SYCP1 might be a functional equivalent of Zip1p, because Sycp1 mutant spermatocytes arrest at approximately the same point as Trip13 mutants, there would be no opportunity to observe bypass of Sycp1 −/−. Since Zip2p is present at sites of axial associations, even in zip1 mutants, it has been suggested that Zip2p promotes initiation of chromosome synapsis [38]. These observations raise the possibility that in yeast, Pch2p responds to synapsis polymerization rather than initiation. To test this, we performed epistasis analysis with a Rec8 allele (Rec8Mei8, abbreviated as Rec8 −). Meiotic chromosomes of Rec8 mutant spermatocytes undergo apparent homolog pairing and interhomolog synaptic initiation, but are defective in DSB repair and fail to maintain interhomolog synapsis [39,40]. Rather, sister chromatids appear to synapse and are bound by SYCP1 along their axes. Rec8 mutants do not progress to diplonema or metaphase I. Double mutant analysis indicated that Rec8 is epistatic to Trip13. As in the Spo11 and Mei1 experiments, histology of testes deficient for both REC8 and TRIP13 resembled the Rec8 mutant, with no evidence of progression to metaphase I that occurs in Trip13Gt/Gt mice (Figure 3L and 3M). Immunocytological analysis of spread chromosomes showed a failure of homologous chromosome synapsis in both the Rec8 −/− and Rec8 −/− Trip13Gt/Gt spermatocytes, as previously reported for Rec8 mutants (Figure 5D and 5E) [39,40]."}

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yeast, deletion of PCH2 alleviates the pachytene arrest caused by asynaptic mutants zip1 and zip2 [8]. Although mouse SYCP1 might be a functional equivalent of Zip1p, because Sycp1 mutant spermatocytes arrest at approximately the same point as Trip13 mutants, there would be no opportunity to observe bypass of Sycp1 −/−. Since Zip2p is present at sites of axial associations, even in zip1 mutants, it has been suggested that Zip2p promotes initiation of chromosome synapsis [38]. These observations raise the possibility that in yeast, Pch2p responds to synapsis polymerization rather than initiation. To test this, we performed epistasis analysis with a Rec8 allele (Rec8Mei8, abbreviated as Rec8 −). Meiotic chromosomes of Rec8 mutant spermatocytes undergo apparent homolog pairing and interhomolog synaptic initiation, but are defective in DSB repair and fail to maintain interhomolog synapsis [39,40]. Rather, sister chromatids appear to synapse and are bound by SYCP1 along their axes. Rec8 mutants do not progress to diplonema or metaphase I. Double mutant analysis indicated that Rec8 is epistatic to Trip13. As in the Spo11 and Mei1 experiments, histology of testes deficient for both REC8 and TRIP13 resembled the Rec8 mutant, with no evidence of progression to metaphase I that occurs in Trip13Gt/Gt mice (Figure 3L and 3M). Immunocytological analysis of spread chromosomes showed a failure of homologous chromosome synapsis in both the Rec8 −/− and Rec8 −/− Trip13Gt/Gt spermatocytes, as previously reported for Rec8 mutants (Figure 5D and 5E) [39,40]."}