The Experts below are selected from a list of 3984 Experts worldwide ranked by ideXlab platform
Maud Borensztein - One of the best experts on this subject based on the ideXlab platform.
-
contribution of epigenetic landscapes and transcription factors to x Chromosome reactivation in the inner cell mass
Nature Communications, 2017Co-Authors: Maud Borensztein, Ikuhiro Okamoto, Laurene Syx, Guillaume Guilbaud, Christel Picard, Katia Ancelin, Rafael Galupa, Patricia DiabangouayaAbstract:X-Chromosome inactivation is established during early development. In mice, transcriptional repression of the paternal X-Chromosome (Xp) and enrichment in epigenetic marks such as H3K27me3 is achieved by the early blastocyst stage. X-Chromosome inactivation is then reversed in the inner cell mass. The mechanisms underlying Xp reactivation remain enigmatic. Using in vivo single-cell approaches (allele-specific RNAseq, nascent RNA-fluorescent in situ hybridization and immunofluorescence), we show here that different genes are reactivated at different stages, with more slowly reactivated genes tending to be enriched in H3meK27. We further show that in UTX H3K27 histone demethylase mutant embryos, these genes are even more slowly reactivated, suggesting that these genes carry an epigenetic memory that may be actively lost. On the other hand, eXpression of rapidly reactivated genes may be driven by transcription factors. Thus, some X-linked genes have minimal epigenetic memory in the inner cell mass, whereas others may require active erasure of chromatin marks.
-
differential epigenetic landscapes and transcription factors eXplain x linked gene behaviours during x Chromosome reactivation in the mouse inner cell mass
bioRxiv, 2017Co-Authors: Maud Borensztein, Ikuhiro Okamoto, Laurene Syx, Guillaume Guilbaud, Christel Picard, Katia Ancelin, Rafael Galupa, Patricia Dianbangouaya, Nicolas Servant, Emmanuel BarillotAbstract:X-Chromosome inactivation (XCI) is established in two waves during mouse development. First, silencing of the paternal X Chromosome (Xp) is triggered, with transcriptional repression of most genes and enrichment of epigenetic marks such as H3K27me3 being achieved in all cells by the early blastocyst stage. XCI is then reversed in the inner cell mass (ICM), followed by a second wave of maternal or paternal XCI, in the embryo-proper. Although the role of Xist RNA in triggering XCI is now clear, the mechanisms underlying Xp reactivation in the inner cell mass have remained enigmatic. Here we use in vivo single cell approaches (allele-specific RNAseq, nascent RNA FISH and immunofluorescence) and find that different genes show very different timing of reactivation. We observe that the genes reactivate at different stages and that initial enrichment in H3K27me3 anti-correlates with the speed of reactivation. To define whether this repressive histone mark is lost actively or passively, we investigate embryos mutant for the X-encoded H3K27me3 demethylase, UTX. Xp genes that normally reactivate slowly are retarded in their reactivation in Utx mutants, while those that reactive rapidly are unaffected. Therefore, efficient reprogramming of some X-linked genes in the inner cell mass is very rapid, indicating minimal epigenetic memory and potentially driven by transcription factors, whereas others may require active erasure of chromatin marks such as H3K27me3.
Ikuhiro Okamoto - One of the best experts on this subject based on the ideXlab platform.
-
contribution of epigenetic landscapes and transcription factors to x Chromosome reactivation in the inner cell mass
Nature Communications, 2017Co-Authors: Maud Borensztein, Ikuhiro Okamoto, Laurene Syx, Guillaume Guilbaud, Christel Picard, Katia Ancelin, Rafael Galupa, Patricia DiabangouayaAbstract:X-Chromosome inactivation is established during early development. In mice, transcriptional repression of the paternal X-Chromosome (Xp) and enrichment in epigenetic marks such as H3K27me3 is achieved by the early blastocyst stage. X-Chromosome inactivation is then reversed in the inner cell mass. The mechanisms underlying Xp reactivation remain enigmatic. Using in vivo single-cell approaches (allele-specific RNAseq, nascent RNA-fluorescent in situ hybridization and immunofluorescence), we show here that different genes are reactivated at different stages, with more slowly reactivated genes tending to be enriched in H3meK27. We further show that in UTX H3K27 histone demethylase mutant embryos, these genes are even more slowly reactivated, suggesting that these genes carry an epigenetic memory that may be actively lost. On the other hand, eXpression of rapidly reactivated genes may be driven by transcription factors. Thus, some X-linked genes have minimal epigenetic memory in the inner cell mass, whereas others may require active erasure of chromatin marks.
-
differential epigenetic landscapes and transcription factors eXplain x linked gene behaviours during x Chromosome reactivation in the mouse inner cell mass
bioRxiv, 2017Co-Authors: Maud Borensztein, Ikuhiro Okamoto, Laurene Syx, Guillaume Guilbaud, Christel Picard, Katia Ancelin, Rafael Galupa, Patricia Dianbangouaya, Nicolas Servant, Emmanuel BarillotAbstract:X-Chromosome inactivation (XCI) is established in two waves during mouse development. First, silencing of the paternal X Chromosome (Xp) is triggered, with transcriptional repression of most genes and enrichment of epigenetic marks such as H3K27me3 being achieved in all cells by the early blastocyst stage. XCI is then reversed in the inner cell mass (ICM), followed by a second wave of maternal or paternal XCI, in the embryo-proper. Although the role of Xist RNA in triggering XCI is now clear, the mechanisms underlying Xp reactivation in the inner cell mass have remained enigmatic. Here we use in vivo single cell approaches (allele-specific RNAseq, nascent RNA FISH and immunofluorescence) and find that different genes show very different timing of reactivation. We observe that the genes reactivate at different stages and that initial enrichment in H3K27me3 anti-correlates with the speed of reactivation. To define whether this repressive histone mark is lost actively or passively, we investigate embryos mutant for the X-encoded H3K27me3 demethylase, UTX. Xp genes that normally reactivate slowly are retarded in their reactivation in Utx mutants, while those that reactive rapidly are unaffected. Therefore, efficient reprogramming of some X-linked genes in the inner cell mass is very rapid, indicating minimal epigenetic memory and potentially driven by transcription factors, whereas others may require active erasure of chromatin marks such as H3K27me3.
Patricia Diabangouaya - One of the best experts on this subject based on the ideXlab platform.
-
contribution of epigenetic landscapes and transcription factors to x Chromosome reactivation in the inner cell mass
Nature Communications, 2017Co-Authors: Maud Borensztein, Ikuhiro Okamoto, Laurene Syx, Guillaume Guilbaud, Christel Picard, Katia Ancelin, Rafael Galupa, Patricia DiabangouayaAbstract:X-Chromosome inactivation is established during early development. In mice, transcriptional repression of the paternal X-Chromosome (Xp) and enrichment in epigenetic marks such as H3K27me3 is achieved by the early blastocyst stage. X-Chromosome inactivation is then reversed in the inner cell mass. The mechanisms underlying Xp reactivation remain enigmatic. Using in vivo single-cell approaches (allele-specific RNAseq, nascent RNA-fluorescent in situ hybridization and immunofluorescence), we show here that different genes are reactivated at different stages, with more slowly reactivated genes tending to be enriched in H3meK27. We further show that in UTX H3K27 histone demethylase mutant embryos, these genes are even more slowly reactivated, suggesting that these genes carry an epigenetic memory that may be actively lost. On the other hand, eXpression of rapidly reactivated genes may be driven by transcription factors. Thus, some X-linked genes have minimal epigenetic memory in the inner cell mass, whereas others may require active erasure of chromatin marks.
Zheng Tan - One of the best experts on this subject based on the ideXlab platform.
-
telomeres at the Chromosome Xp might be critical in limiting the proliferative potential of human cells
Experimental Gerontology, 2001Co-Authors: Yuhua Hao, Zheng TanAbstract:Abstract Normal human somatic cells can only divide for a limited number of times. This phenomenon has been regarded as a reflection of individual aging at the cellular level. EXperimental evidences suggest that a cell's division potential is limited by the physical length of telomeres that gradually shorten through successive cell divisions. At present, it is not clear whether such a limit is imposed by the overall shortening of all telomeres or the shortening of certain critical ones. Computer simulations have suggested that among the 92 telomeres in human cells, two specific telomeres might be preferentially involved in such process. Recent eXperiment has shown that in a culture of male human cells, the length of the telomeres at the Chromosome Xp is reserved over the later passages during clonal proliferation. This unique feature, if can be further confirmed in other cells, implies a critical role of the telomeres at Xp in limiting the proliferation capacity of human cells.
Laurene Syx - One of the best experts on this subject based on the ideXlab platform.
-
contribution of epigenetic landscapes and transcription factors to x Chromosome reactivation in the inner cell mass
Nature Communications, 2017Co-Authors: Maud Borensztein, Ikuhiro Okamoto, Laurene Syx, Guillaume Guilbaud, Christel Picard, Katia Ancelin, Rafael Galupa, Patricia DiabangouayaAbstract:X-Chromosome inactivation is established during early development. In mice, transcriptional repression of the paternal X-Chromosome (Xp) and enrichment in epigenetic marks such as H3K27me3 is achieved by the early blastocyst stage. X-Chromosome inactivation is then reversed in the inner cell mass. The mechanisms underlying Xp reactivation remain enigmatic. Using in vivo single-cell approaches (allele-specific RNAseq, nascent RNA-fluorescent in situ hybridization and immunofluorescence), we show here that different genes are reactivated at different stages, with more slowly reactivated genes tending to be enriched in H3meK27. We further show that in UTX H3K27 histone demethylase mutant embryos, these genes are even more slowly reactivated, suggesting that these genes carry an epigenetic memory that may be actively lost. On the other hand, eXpression of rapidly reactivated genes may be driven by transcription factors. Thus, some X-linked genes have minimal epigenetic memory in the inner cell mass, whereas others may require active erasure of chromatin marks.
-
differential epigenetic landscapes and transcription factors eXplain x linked gene behaviours during x Chromosome reactivation in the mouse inner cell mass
bioRxiv, 2017Co-Authors: Maud Borensztein, Ikuhiro Okamoto, Laurene Syx, Guillaume Guilbaud, Christel Picard, Katia Ancelin, Rafael Galupa, Patricia Dianbangouaya, Nicolas Servant, Emmanuel BarillotAbstract:X-Chromosome inactivation (XCI) is established in two waves during mouse development. First, silencing of the paternal X Chromosome (Xp) is triggered, with transcriptional repression of most genes and enrichment of epigenetic marks such as H3K27me3 being achieved in all cells by the early blastocyst stage. XCI is then reversed in the inner cell mass (ICM), followed by a second wave of maternal or paternal XCI, in the embryo-proper. Although the role of Xist RNA in triggering XCI is now clear, the mechanisms underlying Xp reactivation in the inner cell mass have remained enigmatic. Here we use in vivo single cell approaches (allele-specific RNAseq, nascent RNA FISH and immunofluorescence) and find that different genes show very different timing of reactivation. We observe that the genes reactivate at different stages and that initial enrichment in H3K27me3 anti-correlates with the speed of reactivation. To define whether this repressive histone mark is lost actively or passively, we investigate embryos mutant for the X-encoded H3K27me3 demethylase, UTX. Xp genes that normally reactivate slowly are retarded in their reactivation in Utx mutants, while those that reactive rapidly are unaffected. Therefore, efficient reprogramming of some X-linked genes in the inner cell mass is very rapid, indicating minimal epigenetic memory and potentially driven by transcription factors, whereas others may require active erasure of chromatin marks such as H3K27me3.