I was reading up on KCNQ1, which encodes a voltage-gatedpotassium channel, and I discovered that it happens to be onlymaternally expressed. This is regulated by KCNQ1OT1, a non-codingRNA, which is also epigenetically regulated (expressed onlypaternally). Mutations in KCNQ1OT1 are associated withBeckwith-Wiedemann Syndrome (BWS).
Further reading led to the discovery that there are ART-related(assisted reproductive technology) cases of BWS due to loss ofmethylation at KCNQ1.
However, this article found epigenetic stability of KCNQ1OT1methylation in cultured human embryonic stem cells, which leads meto think that KCNQ1 might also have been properly methylated.
So what exactly are assisted reproductive technologies doingthat can disrupt inheritance of epigenetic marks (that culturinghESCs doesn't do)? (Is this understood for any gene?)
I was reading up on KCNQ1, which encodes a voltage-gatedpotassium channel, and I discovered that it happens to be onlymaternally expressed. This is regulated by KCNQ1OT1, a non-codingRNA, which is also epigenetically regulated (expressed onlypaternally). Mutations in KCNQ1OT1 are associated withBeckwith-Wiedemann Syndrome (BWS).
Further reading led to the discovery that there are ART-related(assisted reproductive technology) cases of BWS due to loss ofmethylation at KCNQ1.
However, this article found epigenetic stability of KCNQ1OT1methylation in cultured human embryonic stem cells, which leads meto think that KCNQ1 might also have been properly methylated.
So what exactly are assisted reproductive technologies doingthat can disrupt inheritance of epigenetic marks (that culturinghESCs doesn't do)? (Is this understood for any gene?)
