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Meiotic Prophase in Dmrt7 Mutant Germ Cells\nDefects in chromosome pairing, synapsis, or recombination can trigger pachytene arrest and apoptosis [46]. We therefore examined these events in Dmrt7 mutant testes. To assess homolog synapsis, we used antibodies to SYCP1, a synaptonemal complex transverse element component, and SYCP3, a component of the axial element, which remains on the desynapsed axes during diplonema [47,48]. Formation of synaptonemal complexes in the mutant was indistinguishable from that in wild-type, as indicated by the proper accumulation of SYCP1 (unpublished data) and SYCP3 (Figure 5A). Likewise, the Dmrt7 mutant zygotene spermatocytes showed normal accumulation of the early recombination repair marker RAD51, suggesting that early meiotic recombination is not significantly affected (Figure 5B). Dmrt7 mutant spermatocytes exhibited the expected decline in the presence of RAD51 foci associated with the autosomal synaptonemal complexes (Figure 5B; unpublished data) [49]. The few surviving cells that progressed beyond pachynema also underwent apparently normal desynapsis during diplonema (Figure 5A). From these results, we conclude that chromosomal pairing, synapsis, recombination, and desynapsis during prophase I in Dmrt7 mutant males are grossly normal.\nFigure 5 Normal Synapsis and Recombination in Dmrt7 Mutant Germ Cells\n(A) Testicular cells from Dmrt7 heterozygous (+/−) or homozygous (−/−) mutant mice were spread and stained with antibody to SYCP3 (red). The developmental stages of meiotic prophase based on SYCP3 organization are indicated in each panel. By pachynema, all autosomes are fully synapsed, and the XY bivalent is synapsed only at the pseudoautosomal region in both wild-type and mutant cells.\n(B) Testicular cells in zygonema and pachynema spread and stained with antibodies to RAD51 (green) and SYCP3 (red). Size and distribution of RAD51 foci are similar between wild-type and mutant spermatocytes."}

{"project":"2_test","denotations":[{"id":"17447844-10973068-85805837","span":{"begin":153,"end":155},"obj":"10973068"},{"id":"17447844-3552678-85805838","span":{"begin":427,"end":429},"obj":"3552678"},{"id":"17447844-8289794-85805839","span":{"begin":430,"end":432},"obj":"8289794"},{"id":"17447844-9443891-85805840","span":{"begin":1006,"end":1008},"obj":"9443891"},{"id":"T43439","span":{"begin":153,"end":155},"obj":"10973068"},{"id":"T45648","span":{"begin":427,"end":429},"obj":"3552678"},{"id":"T6109","span":{"begin":430,"end":432},"obj":"8289794"},{"id":"T33109","span":{"begin":1006,"end":1008},"obj":"9443891"}],"text":"Normal Meiotic Prophase in Dmrt7 Mutant Germ Cells\nDefects in chromosome pairing, synapsis, or recombination can trigger pachytene arrest and apoptosis [46]. We therefore examined these events in Dmrt7 mutant testes. To assess homolog synapsis, we used antibodies to SYCP1, a synaptonemal complex transverse element component, and SYCP3, a component of the axial element, which remains on the desynapsed axes during diplonema [47,48]. Formation of synaptonemal complexes in the mutant was indistinguishable from that in wild-type, as indicated by the proper accumulation of SYCP1 (unpublished data) and SYCP3 (Figure 5A). Likewise, the Dmrt7 mutant zygotene spermatocytes showed normal accumulation of the early recombination repair marker RAD51, suggesting that early meiotic recombination is not significantly affected (Figure 5B). Dmrt7 mutant spermatocytes exhibited the expected decline in the presence of RAD51 foci associated with the autosomal synaptonemal complexes (Figure 5B; unpublished data) [49]. The few surviving cells that progressed beyond pachynema also underwent apparently normal desynapsis during diplonema (Figure 5A). From these results, we conclude that chromosomal pairing, synapsis, recombination, and desynapsis during prophase I in Dmrt7 mutant males are grossly normal.\nFigure 5 Normal Synapsis and Recombination in Dmrt7 Mutant Germ Cells\n(A) Testicular cells from Dmrt7 heterozygous (+/−) or homozygous (−/−) mutant mice were spread and stained with antibody to SYCP3 (red). The developmental stages of meiotic prophase based on SYCP3 organization are indicated in each panel. By pachynema, all autosomes are fully synapsed, and the XY bivalent is synapsed only at the pseudoautosomal region in both wild-type and mutant cells.\n(B) Testicular cells in zygonema and pachynema spread and stained with antibodies to RAD51 (green) and SYCP3 (red). Size and distribution of RAD51 foci are similar between wild-type and mutant spermatocytes."}

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We therefore examined these events in Dmrt7 mutant testes. To assess homolog synapsis, we used antibodies to SYCP1, a synaptonemal complex transverse element component, and SYCP3, a component of the axial element, which remains on the desynapsed axes during diplonema [47,48]. Formation of synaptonemal complexes in the mutant was indistinguishable from that in wild-type, as indicated by the proper accumulation of SYCP1 (unpublished data) and SYCP3 (Figure 5A). Likewise, the Dmrt7 mutant zygotene spermatocytes showed normal accumulation of the early recombination repair marker RAD51, suggesting that early meiotic recombination is not significantly affected (Figure 5B). Dmrt7 mutant spermatocytes exhibited the expected decline in the presence of RAD51 foci associated with the autosomal synaptonemal complexes (Figure 5B; unpublished data) [49]. The few surviving cells that progressed beyond pachynema also underwent apparently normal desynapsis during diplonema (Figure 5A). From these results, we conclude that chromosomal pairing, synapsis, recombination, and desynapsis during prophase I in Dmrt7 mutant males are grossly normal.\nFigure 5 Normal Synapsis and Recombination in Dmrt7 Mutant Germ Cells\n(A) Testicular cells from Dmrt7 heterozygous (+/−) or homozygous (−/−) mutant mice were spread and stained with antibody to SYCP3 (red). The developmental stages of meiotic prophase based on SYCP3 organization are indicated in each panel. By pachynema, all autosomes are fully synapsed, and the XY bivalent is synapsed only at the pseudoautosomal region in both wild-type and mutant cells.\n(B) Testicular cells in zygonema and pachynema spread and stained with antibodies to RAD51 (green) and SYCP3 (red). Size and distribution of RAD51 foci are similar between wild-type and mutant spermatocytes."}

{"project":"craft-ca-core-ex-dev","denotations":[{"id":"T11747","span":{"begin":649,"end":657},"obj":"GO:0000238"},{"id":"T11748","span":{"begin":658,"end":671},"obj":"CL:0000017"},{"id":"T11715","span":{"begin":7,"end":14},"obj":"GO:0007126"},{"id":"T11716","span":{"begin":15,"end":23},"obj":"GO:0051324"},{"id":"T11717","span":{"begin":27,"end":32},"obj":"PR_EXT:000006549"},{"id":"T11718","span":{"begin":33,"end":39},"obj":"SO_EXT:sequence_altered_entity_or_alteration_process"},{"id":"T11719","span":{"begin":40,"end":50},"obj":"CL:0000586"},{"id":"T11720","span":{"begin":45,"end":50},"obj":"CL_GO_EXT:cell"},{"id":"T11721","span":{"begin":62,"end":72},"obj":"GO_SO_EXT:chromosome"},{"id":"T11722","span":{"begin":62,"end":80},"obj":"GO:0007129"},{"id":"T11723","span":{"begin":82,"end":90},"obj":"GO:0007129"},{"id":"T11724","span":{"begin":95,"end":108},"obj":"GO_SO_EXT:sequence_rearrangement_process"},{"id":"T11725","span":{"begin":121,"end":130},"obj":"GO:0000239"},{"id":"T11726","span":{"begin":142,"end":151},"obj":"GO:0006915"},{"id":"T11727","span":{"begin":196,"end":201},"obj":"PR_EXT:000006549"},{"id":"T11728","span":{"begin":202,"end":208},"obj":"SO_EXT:sequence_altered_entity_or_alteration_process"},{"id":"T11729","span":{"begin":209,"end":215},"obj":"UBERON:0000473"},{"id":"T11730","span":{"begin":235,"end":243},"obj":"GO:0007129"},{"id":"T11731","span":{"begin":253,"end":263},"obj":"GO:0042571"},{"id":"T11732","span":{"begin":267,"end":272},"obj":"PR_EXT:000015862"},{"id":"T11733","span":{"begin":276,"end":296},"obj":"GO:0000795"},{"id":"T11734","span":{"begin":297,"end":315},"obj":"GO:0000802"},{"id":"T11735","span":{"begin":331,"end":336},"obj":"PR_EXT:000015865"},{"id":"T11736","span":{"begin":357,"end":370},"obj":"GO:0000800"},{"id":"T11737","span":{"begin":395,"end":403},"obj":"GO:0007129"},{"id":"T11738","span":{"begin":416,"end":425},"obj":"GO:0000240"},{"id":"T11739","span":{"begin":435,"end":470},"obj":"GO:0007130"},{"id":"T11740","span":{"begin":448,"end":470},"obj":"GO:0000795"},{"id":"T11741","span":{"begin":478,"end":484},"obj":"SO_EXT:sequence_altered_entity"},{"id":"T11742","span":{"begin":520,"end":529},"obj":"SO_EXT:wild_type_entity_or_quality"},{"id":"T11743","span":{"begin":574,"end":579},"obj":"PR_EXT:000015862"},{"id":"T11744","span":{"begin":603,"end":608},"obj":"PR_EXT:000015865"},{"id":"T11745","span":{"begin":636,"end":641},"obj":"PR_EXT:000006549"},{"id":"T11746","span":{"begin":642,"end":648},"obj":"SO_EXT:sequence_altered_entity_or_alteration_process"},{"id":"T11749","span":{"begin":712,"end":725},"obj":"GO_SO_EXT:sequence_rearrangement_process"},{"id":"T11750","span":{"begin":712,"end":732},"obj":"GO:0000725"},{"id":"T11751","span":{"begin":733,"end":739},"obj":"CHEBI_SO_EXT:molecular_indicator_or_label_or_marker_or_tag"},{"id":"T11752","span":{"begin":740,"end":745},"obj":"PR_EXT:000013672"},{"id":"T11753","span":{"begin":769,"end":776},"obj":"GO:0007126"},{"id":"T11754","span":{"begin":777,"end":790},"obj":"GO_SO_EXT:sequence_rearrangement_process"},{"id":"T11755","span":{"begin":834,"end":839},"obj":"PR_EXT:000006549"},{"id":"T11756","span":{"begin":840,"end":846},"obj":"SO_EXT:sequence_altered_entity_or_alteration_process"},{"id":"T11757","span":{"begin":847,"end":860},"obj":"CL:0000017"},{"id":"T11758","span":{"begin":911,"end":916},"obj":"PR_EXT:000013672"},{"id":"T11759","span":{"begin":942,"end":951},"obj":"GO:0030849"},{"id":"T11760","span":{"begin":952,"end":974},"obj":"GO:0000795"},{"id":"T11761","span":{"begin":1029,"end":1034},"obj":"CL_GO_EXT:cell"},{"id":"T11762","span":{"begin":1058,"end":1067},"obj":"GO:0000239"},{"id":"T11763","span":{"begin":1103,"end":1111},"obj":"GO:0007129"},{"id":"T11764","span":{"begin":1119,"end":1128},"obj":"GO:0000240"},{"id":"T11765","span":{"begin":1179,"end":1190},"obj":"GO_SO_EXT:chromosome"},{"id":"T11766","span":{"begin":1179,"end":1198},"obj":"GO:0007129"},{"id":"T11767","span":{"begin":1200,"end":1208},"obj":"GO:0007129"},{"id":"T11768","span":{"begin":1210,"end":1223},"obj":"GO_SO_EXT:sequence_rearrangement_process"},{"id":"T11769","span":{"begin":1231,"end":1239},"obj":"GO:0007129"},{"id":"T11770","span":{"begin":1247,"end":1257},"obj":"GO:0007128"},{"id":"T11771","span":{"begin":1261,"end":1266},"obj":"PR_EXT:000006549"},{"id":"T11772","span":{"begin":1267,"end":1273},"obj":"SO_EXT:sequence_altered_entity_or_alteration_process"},{"id":"T11773","span":{"begin":1274,"end":1279},"obj":"PATO_UBERON_EXT:male_or_bearer_of_maleness"},{"id":"T29585","span":{"begin":1317,"end":1325},"obj":"GO:0007129"},{"id":"T29586","span":{"begin":1330,"end":1343},"obj":"GO_SO_EXT:sequence_rearrangement_process"},{"id":"T29587","span":{"begin":1347,"end":1352},"obj":"PR_EXT:000006549"},{"id":"T29588","span":{"begin":1353,"end":1359},"obj":"SO_EXT:sequence_altered_entity_or_alteration_process"},{"id":"T29589","span":{"begin":1360,"end":1370},"obj":"CL:0000586"},{"id":"T29590","span":{"begin":1365,"end":1370},"obj":"CL_GO_EXT:cell"},{"id":"T2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Meiotic Prophase in Dmrt7 Mutant Germ Cells\nDefects in chromosome pairing, synapsis, or recombination can trigger pachytene arrest and apoptosis [46]. We therefore examined these events in Dmrt7 mutant testes. To assess homolog synapsis, we used antibodies to SYCP1, a synaptonemal complex transverse element component, and SYCP3, a component of the axial element, which remains on the desynapsed axes during diplonema [47,48]. Formation of synaptonemal complexes in the mutant was indistinguishable from that in wild-type, as indicated by the proper accumulation of SYCP1 (unpublished data) and SYCP3 (Figure 5A). Likewise, the Dmrt7 mutant zygotene spermatocytes showed normal accumulation of the early recombination repair marker RAD51, suggesting that early meiotic recombination is not significantly affected (Figure 5B). Dmrt7 mutant spermatocytes exhibited the expected decline in the presence of RAD51 foci associated with the autosomal synaptonemal complexes (Figure 5B; unpublished data) [49]. The few surviving cells that progressed beyond pachynema also underwent apparently normal desynapsis during diplonema (Figure 5A). From these results, we conclude that chromosomal pairing, synapsis, recombination, and desynapsis during prophase I in Dmrt7 mutant males are grossly normal.\nFigure 5 Normal Synapsis and Recombination in Dmrt7 Mutant Germ Cells\n(A) Testicular cells from Dmrt7 heterozygous (+/−) or homozygous (−/−) mutant mice were spread and stained with antibody to SYCP3 (red). The developmental stages of meiotic prophase based on SYCP3 organization are indicated in each panel. By pachynema, all autosomes are fully synapsed, and the XY bivalent is synapsed only at the pseudoautosomal region in both wild-type and mutant cells.\n(B) Testicular cells in zygonema and pachynema spread and stained with antibodies to RAD51 (green) and SYCP3 (red). Size and distribution of RAD51 foci are similar between wild-type and mutant spermatocytes."}