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H195A
site-directed mutagenesis, mutation of an Fe2+ binding residue, abolishes demethylase activity of dJMJD2(1)/CG15835
G133A
site-directed mutagenesis, the mutation in the catalytic domain abrogates enzyme activity
G138A
site-directed mutagenesis, the mutation in the catalytic domain abrogates enzyme activity
G165A
site-directed mutagenesis, the mutation in the catalytic domain abrogates enzyme activity
G170A
site-directed mutagenesis, the mutation in the catalytic domain abrogates enzyme activity
S288N
site-directed mutagenesis, the mutation in the catalytic domain abrogates enzyme activity
T289B
site-directed mutagenesis, the mutation in the catalytic domain abrogates enzyme activity
D191A
site-directed mutagenesis, the mutant shows about 95%reduced activity with H3K9me3 compared to wild-type, and no activity with H3K36me3
H188A/E190A
site-directed mutagenesis, inactive mutant
I71L
KDM4E mutant, no demethylation of H3K9me2, but the mutant demethylates H3K9me3 to H3K9me2 and H3K9me1 in a similar manner to wild-type KDM4A
I87K
KDM4E mutant, no demethylation of H3K9me2, but the mutant demethylates H3K9me3 to H3K9me2 and H3K9me1 in a similar manner to wild-type KDM4A
N202M
site-directed mutagenesis, a KDM4D demethylase-dead mutant, that binds RNA like the wild-type enzyme
N290A
site-directed mutagenesis, the mutant shows no activity with H3K36me3 and almost no activity with H3K9me3
N290D
site-directed mutagenesis, the mutant shows about 98%reduced activity with H3K9me3 compared to wild-type, and no activity with H3K36me3
N86H
KDM4E mutant, no demethylation of H3K9me2, but the mutant demethylates H3K9me3 to H3K9me2 and H3K9me1 in a similar manner to wild-type KDM4A
Q88K
KDM4E mutant, the mutant shows demethylation of H3K9me2, and the mutant demethylates H3K9me3 to H3K9me2 and H3K9me1 in a similar manner to wild-type KDM4A
R309G
KDM4E mutant, poor demethylation of H3K9me2, but the mutant demethylates H3K9me3 to H3K9me2 and H3K9me1 in a similar manner to wild-type KDM4A
R919D
site-directed mutagenesis, the mutant is not associated with mitotic chromatin in contrast to the wild-type enzyme
S198M
site-directed mutagenesis, a KDM4C demethylase dead mutant
Y175F
site-directed mutagenesis, the mutant shows about 90%reduced activity with H3K9me3 compared to wild-type, and no activity with H3K36me3
Y177F
site-directed mutagenesis, the mutant shows about 90%reduced activity with H3K9me3 compared to wild-type, and no activity with H3K36me3
S288A
mutations of the residues comprising the methylammonium-binding pocket abrogate demethylation by JMJD2A, with the exception of an S288A substitution, which augments activity, particularly toward H3K9me2
S288A
site-directed mutagenesis, the JMJD2A S2888A mutant demonstrates an approximately 12fold increase in H3K9me2 specificity compared to the native enzyme, whereas the converse A291S mutant in JMJD2D reduces H3K9me2 specificity approximately fivefold
additional information
the kdmA mutant shows a significant increase in H3K36me3 during primary metabolism at the aflR and ipnA locus and some slightly higher levels at the aptA genes, the mutant has reduced levels of sterigmatocystin compared to wild-type, mutant phenotype, overview. Deletion of kdmA in Aspergillus nidulans produces both positive and negative changes in transcriptional readouts and the number of affected genes is different under different conditions. KdmA deletion alters expression pattern of secondary metabolism cluster genes in secondary metabolism phase, analysis of the heat map for mean expression of previously annotated secondary metabolism clusters. Deletion of kdmA causes light lethality and sensitivity to oxidative stress during vegetative growth
additional information
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the kdmA mutant shows a significant increase in H3K36me3 during primary metabolism at the aflR and ipnA locus and some slightly higher levels at the aptA genes, the mutant has reduced levels of sterigmatocystin compared to wild-type, mutant phenotype, overview. Deletion of kdmA in Aspergillus nidulans produces both positive and negative changes in transcriptional readouts and the number of affected genes is different under different conditions. KdmA deletion alters expression pattern of secondary metabolism cluster genes in secondary metabolism phase, analysis of the heat map for mean expression of previously annotated secondary metabolism clusters. Deletion of kdmA causes light lethality and sensitivity to oxidative stress during vegetative growth
additional information
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the kdmA mutant shows a significant increase in H3K36me3 during primary metabolism at the aflR and ipnA locus and some slightly higher levels at the aptA genes, the mutant has reduced levels of sterigmatocystin compared to wild-type, mutant phenotype, overview. Deletion of kdmA in Aspergillus nidulans produces both positive and negative changes in transcriptional readouts and the number of affected genes is different under different conditions. KdmA deletion alters expression pattern of secondary metabolism cluster genes in secondary metabolism phase, analysis of the heat map for mean expression of previously annotated secondary metabolism clusters. Deletion of kdmA causes light lethality and sensitivity to oxidative stress during vegetative growth
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additional information
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the kdmA mutant shows a significant increase in H3K36me3 during primary metabolism at the aflR and ipnA locus and some slightly higher levels at the aptA genes, the mutant has reduced levels of sterigmatocystin compared to wild-type, mutant phenotype, overview. Deletion of kdmA in Aspergillus nidulans produces both positive and negative changes in transcriptional readouts and the number of affected genes is different under different conditions. KdmA deletion alters expression pattern of secondary metabolism cluster genes in secondary metabolism phase, analysis of the heat map for mean expression of previously annotated secondary metabolism clusters. Deletion of kdmA causes light lethality and sensitivity to oxidative stress during vegetative growth
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additional information
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the kdmA mutant shows a significant increase in H3K36me3 during primary metabolism at the aflR and ipnA locus and some slightly higher levels at the aptA genes, the mutant has reduced levels of sterigmatocystin compared to wild-type, mutant phenotype, overview. Deletion of kdmA in Aspergillus nidulans produces both positive and negative changes in transcriptional readouts and the number of affected genes is different under different conditions. KdmA deletion alters expression pattern of secondary metabolism cluster genes in secondary metabolism phase, analysis of the heat map for mean expression of previously annotated secondary metabolism clusters. Deletion of kdmA causes light lethality and sensitivity to oxidative stress during vegetative growth
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additional information
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the kdmA mutant shows a significant increase in H3K36me3 during primary metabolism at the aflR and ipnA locus and some slightly higher levels at the aptA genes, the mutant has reduced levels of sterigmatocystin compared to wild-type, mutant phenotype, overview. Deletion of kdmA in Aspergillus nidulans produces both positive and negative changes in transcriptional readouts and the number of affected genes is different under different conditions. KdmA deletion alters expression pattern of secondary metabolism cluster genes in secondary metabolism phase, analysis of the heat map for mean expression of previously annotated secondary metabolism clusters. Deletion of kdmA causes light lethality and sensitivity to oxidative stress during vegetative growth
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additional information
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the kdmA mutant shows a significant increase in H3K36me3 during primary metabolism at the aflR and ipnA locus and some slightly higher levels at the aptA genes, the mutant has reduced levels of sterigmatocystin compared to wild-type, mutant phenotype, overview. Deletion of kdmA in Aspergillus nidulans produces both positive and negative changes in transcriptional readouts and the number of affected genes is different under different conditions. KdmA deletion alters expression pattern of secondary metabolism cluster genes in secondary metabolism phase, analysis of the heat map for mean expression of previously annotated secondary metabolism clusters. Deletion of kdmA causes light lethality and sensitivity to oxidative stress during vegetative growth
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additional information
construction of transgenic lines carrying a UASGAL4-CG15835-Flag construct, where expression of dJMJD2(1)/CG15835 is under the control of the yeast activator GAL4, allowing its overexpression upon crossing with lines expressing GAL4. Overexpression of CG15835 results in spreading of HP1 into euchromatin and a strong decrease on the levels of H3K9me3 and H3K36me3
additional information
construction of transgenic lines carrying a UASGAL4-CG15835-Flag construct, where expression of dJMJD2(1)/CG15835 is under the control of the yeast activator GAL4, allowing its overexpression upon crossing with lines expressing GAL4. Overexpression of CG15835 results in spreading of HP1 into euchromatin and a strong decrease on the levels of H3K9me3 and H3K36me3
additional information
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construction of transgenic lines carrying a UASGAL4-CG15835-Flag construct, where expression of dJMJD2(1)/CG15835 is under the control of the yeast activator GAL4, allowing its overexpression upon crossing with lines expressing GAL4. Overexpression of CG15835 results in spreading of HP1 into euchromatin and a strong decrease on the levels of H3K9me3 and H3K36me3
additional information
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overexpression of JmjD2A in fibroblasts specifically depletes H3K9me3 and H3K36me3. Loss of JmjD2A by knockdown leads to depletion of neural crest specifier genes, but causes no significant changes in the expression of several neural tube, ectodermal, neural plate, and border genes, or in markers of proliferation and apoptosis, overview
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overexpression of JmjD2A in fibroblasts specifically depletes H3K9me3 and H3K36me3
additional information
mutation of R2, Q5, and D555 lead to enzyme inactivation
additional information
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siRNA induced enzyme knockdown causes a decrease in the level of H3K9me3 at the promoters of ERalpha targets TFF1 and EBAG9
additional information
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siRNA silencing of DELTAN-JMJD2A results in drastic impairment of MHC expression and myotube formation, the Myog promoter is a specific target of DElTAN-JMJD2A. Genome-wide expression profiling and exon-specific siRNA knockdown indicate that, in contrast to the full-length protein, N-terminal demethylase domainis necessary for myotube formation and muscle-specific gene expression
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enzyme knockout by expression of siRNA targeting JMJD2B in 3T3-L1 preadipocytes
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generation of the truncated enzyme variant KDM4A1?359
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enzyme engineering and swapping of the C-terminus region containing the distal Tudor domain between isozymes KDM4C and KDM4A, construction of diverse chimeric enzyme mutants, overview. Chimera5, which encodes the first 934 amino acids of KDM4C fused with the last 129 amino acid containing the distal Tudor domain of KDM4A, is excluded from mitotic chromatin. On the other hand, chimera6 that encodes the first 954 amino acids of KDM4A fused to 101 amino acids of KDM4C, which includes its distal Tudor domain, remains excluded from chromatin. The C-terminus of KDM4C containing the distal Tudor domain is essential but not sufficient for its mitotic chromatin localization
additional information
enzyme engineering and swapping of the C-terminus region containing the distal Tudor domain between isozymes KDM4C and KDM4A, construction of diverse chimeric enzyme mutants, overview. Chimera5, which encodes the first 934 amino acids of KDM4C fused with the last 129 amino acid containing the distal Tudor domain of KDM4A, is excluded from mitotic chromatin. On the other hand, chimera6 that encodes the first 954 amino acids of KDM4A fused to 101 amino acids of KDM4C, which includes its distal Tudor domain, remains excluded from chromatin. The C-terminus of KDM4C containing the distal Tudor domain is essential but not sufficient for its mitotic chromatin localization
additional information
enzyme engineering and swapping of the C-terminus region containing the distal Tudor domain between isozymes KDM4C and KDM4A, construction of diverse chimeric enzyme mutants, overview. Chimera5, which encodes the first 934 amino acids of KDM4C fused with the last 129 amino acid containing the distal Tudor domain of KDM4A, is excluded from mitotic chromatin. On the other hand, chimera6 that encodes the first 954 amino acids of KDM4A fused to 101 amino acids of KDM4C, which includes its distal Tudor domain, remains excluded from chromatin. The C-terminus of KDM4C containing the distal Tudor domain is essential but not sufficient for its mitotic chromatin localization
additional information
enzyme engineering and swapping of the C-terminus region containing the distal Tudor domain between isozymes KDM4C and KDM4A, construction of diverse chimeric enzyme mutants, overview. Chimera5, which encodes the first 934 amino acids of KDM4C fused with the last 129 amino acid containing the distal Tudor domain of KDM4A, is excluded from mitotic chromatin. On the other hand, chimera6 that encodes the first 954 amino acids of KDM4A fused to 101 amino acids of KDM4C, which includes its distal Tudor domain, remains excluded from chromatin. The C-terminus of KDM4C containing the distal Tudor domain is essential but not sufficient for its mitotic chromatin localization. EGFP-KDM4CRDTF/DNLY mutant is excluded from mitotic chromatin. For isozyme knockout, U2OS cells are transfected with KDM4B-C siRNA sequences
additional information
enzyme engineering and swapping of the C-terminus region containing the distal Tudor domain between isozymes KDM4C and KDM4A, construction of diverse chimeric enzyme mutants, overview. Chimera5, which encodes the first 934 amino acids of KDM4C fused with the last 129 amino acid containing the distal Tudor domain of KDM4A, is excluded from mitotic chromatin. On the other hand, chimera6 that encodes the first 954 amino acids of KDM4A fused to 101 amino acids of KDM4C, which includes its distal Tudor domain, remains excluded from chromatin. The C-terminus of KDM4C containing the distal Tudor domain is essential but not sufficient for its mitotic chromatin localization. EGFP-KDM4CRDTF/DNLY mutant is excluded from mitotic chromatin. For isozyme knockout, U2OS cells are transfected with KDM4B-C siRNA sequences
additional information
enzyme engineering and swapping of the C-terminus region containing the distal Tudor domain between isozymes KDM4C and KDM4A, construction of diverse chimeric enzyme mutants, overview. Chimera5, which encodes the first 934 amino acids of KDM4C fused with the last 129 amino acid containing the distal Tudor domain of KDM4A, is excluded from mitotic chromatin. On the other hand, chimera6 that encodes the first 954 amino acids of KDM4A fused to 101 amino acids of KDM4C, which includes its distal Tudor domain, remains excluded from chromatin. The C-terminus of KDM4C containing the distal Tudor domain is essential but not sufficient for its mitotic chromatin localization. EGFP-KDM4CRDTF/DNLY mutant is excluded from mitotic chromatin. For isozyme knockout, U2OS cells are transfected with KDM4B-C siRNA sequences
additional information
expression profiling of C2C12 cells following transfection with siRNAs against both isoforms of JMJD2A, transfected C2C12 cells with siRNAs that target exon 9 or exon 10 (sie9 and sie10) are maintained in proliferation medium for 24 h before shifting them to differentiation medium for 36 hours. The siRNAs do not affect JMJD2B and JMJD2C mRNA. Genes Actc1, Tnni1, Ttn, Myog, and Ckm, are considered as deregulated upon JMJD2A knockdown, as compared to a control siRNA
additional information
JMJD2A knockout or overexpression in Hep-3B cells. Construction of JMJD2ADELTA mutant. A 39KD JMJD2A transcript, JMJD2ADELTA, is significantly increased in JMJD2A or miR372 overexpressing Hep3B cell line
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Jmjd2b knockdown by siRNA, leading to induction of p53 via activation of the DNA damage response pathway. p53 Inhibition significantly restored the clonogenic potential of AGS and HeLa cells treated with JMJD2B siRNA. Increased apoptosis in BGC-823 and HeLa cells but not AGS cells with JMJD2B siRNA knockdown. AGS cells are arrested at the G1 phase, but BGC-823 and HeLa cells are arrested at the S phase
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mutations of the G12-G13 motif abrogating H3K9me3 demethylation by JMJD2A. Introduction of a di-glycine motif at the +3 to +4 positions of the H3K27 sequence, a site which shares sequence homology with the H3K9 sequence, enables JMJD2A to efficiently demethylate H3K27me3, cf. EC 1.14.11.68
additional information
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mutant and truncated forms of JMJD2b densely occupy the nucleolar compartment of fibroblasts. The PHD Zn-fingers and Tudor domains are removed in truncated JMJD2b. Nuclear patterns of full-length JMJD2b in comparison with truncated and mutated forms of JMJD2b, overview
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generation of Kdm3b knockout (Kdm3bKO) mice, phenotype, overview. female Kdm3bKO mice exhibit a severely impaired reproductive function, knockout of Kdm3b increases the levels of H3K9me1, H3K9me2 and H3K9me3 in the ovary and uterus. Knockout of Kdm3b in female mice prolonges their estrous cycles and reduces their ovulation capacity and fertilization efficiency
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construction of Jmjd2c knockout embryonic stem cells by RNAi assay, Jmjd2c depletion leads to embryonic stem cell differentiation, which is accompanied by a reduction in the expression of embryonic stem cell-specific genes and an induction of lineage marker genes. The same mutations that disrupt the in vitro Oct4/DNA interactions also abolished the enhancer activities. Knockdown of Jmjd1a does not appreciably affect Jmjd2c and vice versa
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generation of conditional Jmjd2a/Kdm4a, Jmjd2b/Kdm4b and Jmjd2c/Kdm4c/Gasc1 single, double and triple knockout mouse embryonic stem cells (ESCs). While individual Jmjd2 family members are dispensable for ESC maintenance and embryogenesis, combined deficiency for specifically Jmjd2a and Jmjd2c leads to early embryonic lethality and impaired ESC self-renewal, with spontaneous differentiation towards primitive endoderm under permissive culture conditions. Increased H3K9me3 levels in knockout ESCs compromise the expression of several Jmjd2a/c targets, including genes that are important for ESC self-renewal. Thus, continual removal of H3K9 promoter methylation by Jmjd2 demethylases represents a novel mechanism ensuring transcriptional competence and stability of the pluripotent cell identity. Phenotypes, overview
additional information
generation of conditional Jmjd2a/Kdm4a, Jmjd2b/Kdm4b and Jmjd2c/Kdm4c/Gasc1 single, double and triple knockout mouse embryonic stem cells (ESCs). While individual Jmjd2 family members are dispensable for ESC maintenance and embryogenesis, combined deficiency for specifically Jmjd2a and Jmjd2c leads to early embryonic lethality and impaired ESC self-renewal, with spontaneous differentiation towards primitive endoderm under permissive culture conditions. Increased H3K9me3 levels in knockout ESCs compromise the expression of several Jmjd2a/c targets, including genes that are important for ESC self-renewal. Thus, continual removal of H3K9 promoter methylation by Jmjd2 demethylases represents a novel mechanism ensuring transcriptional competence and stability of the pluripotent cell identity. Phenotypes, overview
additional information
generation of conditional Jmjd2a/Kdm4a, Jmjd2b/Kdm4b and Jmjd2c/Kdm4c/Gasc1 single, double and triple knockout mouse embryonic stem cells (ESCs). While individual Jmjd2 family members are dispensable for ESC maintenance and embryogenesis, combined deficiency for specifically Jmjd2a and Jmjd2c leads to early embryonic lethality and impaired ESC self-renewal, with spontaneous differentiation towards primitive endoderm under permissive culture conditions. Increased H3K9me3 levels in knockout ESCs compromise the expression of several Jmjd2a/c targets, including genes that are important for ESC self-renewal. Thus, continual removal of H3K9 promoter methylation by Jmjd2 demethylases represents a novel mechanism ensuring transcriptional competence and stability of the pluripotent cell identity. Phenotypes, overview
additional information
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generation of conditional Jmjd2a/Kdm4a, Jmjd2b/Kdm4b and Jmjd2c/Kdm4c/Gasc1 single, double and triple knockout mouse embryonic stem cells (ESCs). While individual Jmjd2 family members are dispensable for ESC maintenance and embryogenesis, combined deficiency for specifically Jmjd2a and Jmjd2c leads to early embryonic lethality and impaired ESC self-renewal, with spontaneous differentiation towards primitive endoderm under permissive culture conditions. Increased H3K9me3 levels in knockout ESCs compromise the expression of several Jmjd2a/c targets, including genes that are important for ESC self-renewal. Thus, continual removal of H3K9 promoter methylation by Jmjd2 demethylases represents a novel mechanism ensuring transcriptional competence and stability of the pluripotent cell identity. Phenotypes, overview
additional information
generation of Jmjd2b-knockdown (kd) NE-4C cells. Jmjd2b-kd can inhibit the Notch1, IL-1beta, and IL-2 genes by recruiting repressive H3K9me3 to their promoter. attenuation of Jmjd2b by si RNA, increases expression of Jmjd3, the H3K27me3 demethylase, and of Ccl2, overview. Jmjd2b attenuation inhibits the gene expression of p65, inducible nitric oxide synthase, B cell lymphoma 2, and transforming growth factor beta in Jmjd2b-kd NE-4C cells
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generation of Jmjd2b-knockdown (kd) NE-4C cells. Jmjd2b-kd can inhibit the Notch1, IL-1beta, and IL-2 genes by recruiting repressive H3K9me3 to their promoter. attenuation of Jmjd2b by si RNA, increases expression of Jmjd3, the H3K27me3 demethylase, and of Ccl2, overview. Jmjd2b attenuation inhibits the gene expression of p65, inducible nitric oxide synthase, B cell lymphoma 2, and transforming growth factor beta in Jmjd2b-kd NE-4C cells
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targeted disruption of KDM4D, a testis-enriched tridemethylase of H3K9. Kdm4d-null mice are viable and fertile and do not show any obvious phenotype, but H3K9me3 accumulates significantly in Kdm4d-null round spermatids, and the distribution of methylated H3K9 in germ cells is dramatically changed, overview. Lack of expression of Kdm4d in spermatogonia is consistent with lack of expression of Kdm4d in germline stem cells
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targeted disruption of KDM4D, a testis-enriched tridemethylase of H3K9. Kdm4d-null mice are viable and fertile and do not show any obvious phenotype, but H3K9me3 accumulates significantly in Kdm4d-null round spermatids, and the distribution of methylated H3K9 in germ cells is dramatically changed, overview. Lack of expression of Kdm4d in spermatogonia is consistent with lack of expression of Kdm4d in germline stem cells
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generation of Kdm3b knockout (Kdm3bKO) mice, phenotype, overview. female Kdm3bKO mice exhibit a severely impaired reproductive function, knockout of Kdm3b increases the levels of H3K9me1, H3K9me2 and H3K9me3 in the ovary and uterus. Knockout of Kdm3b in female mice prolonges their estrous cycles and reduces their ovulation capacity and fertilization efficiency
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additional information
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generation of conditional Jmjd2a/Kdm4a, Jmjd2b/Kdm4b and Jmjd2c/Kdm4c/Gasc1 single, double and triple knockout mouse embryonic stem cells (ESCs). While individual Jmjd2 family members are dispensable for ESC maintenance and embryogenesis, combined deficiency for specifically Jmjd2a and Jmjd2c leads to early embryonic lethality and impaired ESC self-renewal, with spontaneous differentiation towards primitive endoderm under permissive culture conditions. Increased H3K9me3 levels in knockout ESCs compromise the expression of several Jmjd2a/c targets, including genes that are important for ESC self-renewal. Thus, continual removal of H3K9 promoter methylation by Jmjd2 demethylases represents a novel mechanism ensuring transcriptional competence and stability of the pluripotent cell identity. Phenotypes, overview
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additional information
a JMJ706 loss-of-function mutation affects floral organogenesis, construction of knockout mutants that show altered content and ratios of methylated histone H3K9, overview
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a JMJ706 loss-of-function mutation affects floral organogenesis, construction of knockout mutants that show altered content and ratios of methylated histone H3K9, overview