Thank you for making me so wonderfully complex! Psalm 139:14
".......scientists at Harvard Medical School (HMS) and Boston Children’s Hospital have identified a mechanism that regulates the imprinting of multiple genes, including some of those critical to placental growth during early embryonic development in mice. The results were reported yesterday in Nature.
“A gene that is turned off by epigenetic modifications can be turned on much more easily than a gene that is mutated or missing can be fixed,” said Yi Zhang.
Genomic imprinting is an epigenetic process that contributes to embryonic development by silencing the gene from one parent — effectively turning the gene off — in the offspring.
Zhang’s team was mapping imprinted genomic regions in early-stage mouse embryos, when they noticed mysterious DNA methylation-independent imprinted regions.
“Much to our surprise, the imprinted genes we looked at lacked DNA methylation, which told us there must be another mechanism at play,” Inoue said.
Zhang’s team dug deeper into the genomic regions and discovered the consistent presence of H3K27me3, a chemical modification to the genes’ histones, proteins that form the spool around which the thread of DNA is wound.
This histone modification had previously been identified as an epigenetic gene silencing mechanism in other scenarios, but not as a regulator of imprinting, the researchers say. They demonstrated that not only was the histone modification necessary for imprinting certain genes, but that DNA methylation played no role in imprinting them.
In other words, the researchers said, the DNA methylation-independent imprinted genes identified by researchers in the recent past were, in fact, regulated by H3K27me3.
In all, the researchers identified 76 genes potentially imprinted by histone modification rather than by DNA methylation. This set of imprinted genes includes several linked to placental development, limb abnormalities and a disorder associated with severe eye anomalies.
The findings could lead to development of epigenetic therapies for a range of devastating developmental disorders, Zhang’s team said."
Vector/BostonChildren'sHospital
".......scientists at Harvard Medical School (HMS) and Boston Children’s Hospital have identified a mechanism that regulates the imprinting of multiple genes, including some of those critical to placental growth during early embryonic development in mice. The results were reported yesterday in Nature.
“A gene that is turned off by epigenetic modifications can be turned on much more easily than a gene that is mutated or missing can be fixed,” said Yi Zhang.
Genomic imprinting is an epigenetic process that contributes to embryonic development by silencing the gene from one parent — effectively turning the gene off — in the offspring.
Zhang’s team was mapping imprinted genomic regions in early-stage mouse embryos, when they noticed mysterious DNA methylation-independent imprinted regions.
“Much to our surprise, the imprinted genes we looked at lacked DNA methylation, which told us there must be another mechanism at play,” Inoue said.
Zhang’s team dug deeper into the genomic regions and discovered the consistent presence of H3K27me3, a chemical modification to the genes’ histones, proteins that form the spool around which the thread of DNA is wound.
This histone modification had previously been identified as an epigenetic gene silencing mechanism in other scenarios, but not as a regulator of imprinting, the researchers say. They demonstrated that not only was the histone modification necessary for imprinting certain genes, but that DNA methylation played no role in imprinting them.
In other words, the researchers said, the DNA methylation-independent imprinted genes identified by researchers in the recent past were, in fact, regulated by H3K27me3.
In all, the researchers identified 76 genes potentially imprinted by histone modification rather than by DNA methylation. This set of imprinted genes includes several linked to placental development, limb abnormalities and a disorder associated with severe eye anomalies.
The findings could lead to development of epigenetic therapies for a range of devastating developmental disorders, Zhang’s team said."
Vector/BostonChildren'sHospital
