MES GENES ARE NEEDED FOR GERM-LINE VIABILITY IN A SEX-CHROMOSOME-DEPENDENT MANNER Export

@inproceedings{citeulike:3311482, abstract = {We have identified four maternal-effect sterile genes, mes-2, mes-3, mes-4, and mes-6, that encode maternal components required for normal post-embryonic development of the germ line. mes mutant mothers produce sterile hermaphrodite progeny, which contain few germ cells and no gametes. We previously observed that the number of DAPI-stained germ nuclei increases and then declines. This appears to be due to germ cell death, characterized mainly by swelling of the nuclei and "coagulation" of the cytoplasm, in L3 and later stage worms. The appearance of the dying cells suggests a degeneration type of death and not programmed cell death. Consistent with this, germ-cell death and maternal-effect sterility are not suppressed by mutations in ced-3 or ced-4, which suppress other programmed cell deaths in C. elegans. Thus, the mes gene products are required for germ cell viability. Male progeny of mes mutant mothers usually have substantially healthier germ lines than hermaphrodite progeny. In fact, mutant males often produce sperm and can be fertile. To test which aspect(s) of the male vs. hermaphrodite state (germ-line sex, somatic gonad, or X:A ratio) is responsible for the difference between mes hermaphrodite vs. male germ-line development, we have genetically altered the somatic and/or germ-line sex of XX and XO mes animals. Our results indicate that, regardless of the germ-line or somatic sex of the animals, XO animals generally have more proliferated and healthier germ lines than XX animals. The correlation is particularly striking with mes-4, but is also observed with the other mes mutants. These findings suggest a role for the mes genes in control of X chromosome gene expression. The mes genes may control dosage compensation in the germ line, or they may protect the germ line from an absence of dosage compensation.}, author = {Garvin, C. M. and Paulsen, J. E. and Strome, S.}, citeulike-article-id = {3311482}, citeulike-linkout-0 = {http://www.wormbase.org/db/misc/paper?name=WBPaper00022139}, journal = {International C. elegans Meeting}, keywords = {c09g45, c35d109, c48d12, c\_elegans, caenorhabditis\_elegans, ced-3, ced-4, celegans, elegans, f54c13, meeting\_abstract, mes-2, mes-3, mes-4, mes-6, nematode, r06a47, wormbase, y2h9a1}, posted-at = {2008-09-21 21:43:10}, priority = {3}, title = {MES GENES ARE NEEDED FOR GERM-LINE VIABILITY IN A SEX-CHROMOSOME-DEPENDENT MANNER}, url = {http://www.wormbase.org/db/misc/paper?name=WBPaper00022139}, year = {1995} }

TY - CONF ID - citeulike:3311482 L3 - citeulike-article-id:3311482 N2 - We have identified four maternal-effect sterile genes, mes-2, mes-3, mes-4, and mes-6, that encode maternal components required for normal post-embryonic development of the germ line. mes mutant mothers produce sterile hermaphrodite progeny, which contain few germ cells and no gametes. We previously observed that the number of DAPI-stained germ nuclei increases and then declines. This appears to be due to germ cell death, characterized mainly by swelling of the nuclei and "coagulation" of the cytoplasm, in L3 and later stage worms. The appearance of the dying cells suggests a degeneration type of death and not programmed cell death. Consistent with this, germ-cell death and maternal-effect sterility are not suppressed by mutations in ced-3 or ced-4, which suppress other programmed cell deaths in C. elegans. Thus, the mes gene products are required for germ cell viability. Male progeny of mes mutant mothers usually have substantially healthier germ lines than hermaphrodite progeny. In fact, mutant males often produce sperm and can be fertile. To test which aspect(s) of the male vs. hermaphrodite state (germ-line sex, somatic gonad, or X:A ratio) is responsible for the difference between mes hermaphrodite vs. male germ-line development, we have genetically altered the somatic and/or germ-line sex of XX and XO mes animals. Our results indicate that, regardless of the germ-line or somatic sex of the animals, XO animals generally have more proliferated and healthier germ lines than XX animals. The correlation is particularly striking with mes-4, but is also observed with the other mes mutants. These findings suggest a role for the mes genes in control of X chromosome gene expression. The mes genes may control dosage compensation in the germ line, or they may protect the germ line from an absence of dosage compensation. JF - International C. elegans Meeting TI - MES GENES ARE NEEDED FOR GERM-LINE VIABILITY IN A SEX-CHROMOSOME-DEPENDENT MANNER KW - c09g45 KW - c35d109 KW - c48d12 KW - c_elegans KW - caenorhabditis_elegans KW - ced-3 KW - ced-4 KW - celegans KW - elegans KW - f54c13 KW - meeting_abstract KW - mes-2 KW - mes-3 KW - mes-4 KW - mes-6 KW - nematode KW - r06a47 KW - wormbase KW - y2h9a1 AU - Garvin, CM AU - Paulsen, JE AU - Strome, S PY - 1995/// UR - http://www.wormbase.org/db/misc/paper?name=WBPaper00022139 ER -