Very nice and interesting data, relevant to some rare human cancer diseases, eventhough initial research was literally based upon yeast models! I admire Dr. Allis and his co-workers. He's one of the best in epigenomics research, hands down.
I'm taking a class on epigenetics and it has been quite confusing for me. But his explanations here are clear and so relevant. He should do more public lectures!
I learned a lot and it's a history of great work, but from the beginning of the first lecture to the end of the second, the focus keeps narrowing from "epigenetics in development and disease" to a few rare cancers. Anyone interested in large public health problems like the global epidemic of type 2 diabetes and the racial and social disparities in COVID-19 severity would appreciate a mention of the known causal role of epigenetics in susceptibility to diabetes and, by extension, COVID-19.
He linked "Nature" to the death of Steve Jobs, and oncohistones to the death of us all from virus-driven pathology. I expected more focus on biophysically constrained RNA-mediated protein folding chemistry and the amino acid substitutions that stabilize the energy-dependent organized genomes of all living genera. He seems to have abandoned the context in: "Every amino acid matters: essential contributions of histone variants to mammalian development and disease" www.ncbi.nlm.nih.gov/pmc/articles/PMC4082118/ Now, every amino acid is placed into the context of oncohistones and pathology. The clarity of facts that link the innate immune system from supercoiled DNA to protection from virus-driven energy theft via RNA methylation has been eliminated. Perhaps that is why the second lecture is less clear.
Maybe all the K27I thing indicates K27M and K27I are the only post-natal survivors. Also the H3.3 to the ends of transcription as a general binding for somekind of histone supercoiling tension thing. instead of a pressure ....
I wonder if there's really something that makes mutations of H3.3K27 → I harder to happen than H3.3K27 → M. Or, is there something that makes K27 → M mutations more destructive that K27 → I? It also makes sense that damaging one amino acid in the region that controls the enabling and disabling of a gene would be a lot more impactful than damaging one amino acid in a protein used for other purposes. If you permanently disable all the codons wrapped around a nucleosome, or can't control when they should stop being expressed, you've pretty much impacted all the hundreds of codons around that nucleosome, or, perhaps, even the whole gene. (Also, how is enabling and disabling of all the nucleosomes that are part of the same gene coordinated?) It also makes intuitive sense that being unable to regulate the expression of a gene can result in uncontrolled growth. E.g., if you can't produce a signal that plays a role in telling the cell, or other cells to stop dividing, you'd expect to get uncontrolled tissue growth.
Very nice and interesting data, relevant to some rare human cancer diseases, eventhough initial research was literally based upon yeast models! I admire Dr. Allis and his co-workers. He's one of the best in epigenomics research, hands down.
I'm taking a class on epigenetics and it has been quite confusing for me. But his explanations here are clear and so relevant. He should do more public lectures!
Can you please tell when do biology students have to study epigenetics like in the video . to get bachelor degree ? Master degree ..?
I love that these videos are available, and i really hope more is produced as the research is continued.
I learned a lot and it's a history of great work, but from the beginning of the first lecture to the end of the second, the focus keeps narrowing from "epigenetics in development and disease" to a few rare cancers. Anyone interested in large public health problems like the global epidemic of type 2 diabetes and the racial and social disparities in COVID-19 severity would appreciate a mention of the known causal role of epigenetics in susceptibility to diabetes and, by extension, COVID-19.
David's first lecture was very clear, the second less so....His lab is doing great things and he is clearly doing pioneering work...
He linked "Nature" to the death of Steve Jobs, and oncohistones to the death of us all from virus-driven pathology. I expected more focus on biophysically constrained RNA-mediated protein folding chemistry and the amino acid substitutions that stabilize the energy-dependent organized genomes of all living genera.
He seems to have abandoned the context in: "Every amino acid matters: essential contributions of histone variants to mammalian development and disease" www.ncbi.nlm.nih.gov/pmc/articles/PMC4082118/
Now, every amino acid is placed into the context of oncohistones and pathology. The clarity of facts that link the innate immune system from supercoiled DNA to protection from virus-driven energy theft via RNA methylation has been eliminated. Perhaps that is why the second lecture is less clear.
Maybe all the K27I thing indicates K27M and K27I are the only post-natal survivors. Also the H3.3 to the ends of transcription as a general binding for somekind of histone supercoiling tension thing. instead of a pressure ....
I wonder if there's really something that makes mutations of H3.3K27 → I harder to happen than H3.3K27 → M. Or, is there something that makes K27 → M mutations more destructive that K27 → I?
It also makes sense that damaging one amino acid in the region that controls the enabling and disabling of a gene would be a lot more impactful than damaging one amino acid in a protein used for other purposes. If you permanently disable all the codons wrapped around a nucleosome, or can't control when they should stop being expressed, you've pretty much impacted all the hundreds of codons around that nucleosome, or, perhaps, even the whole gene. (Also, how is enabling and disabling of all the nucleosomes that are part of the same gene coordinated?)
It also makes intuitive sense that being unable to regulate the expression of a gene can result in uncontrolled growth. E.g., if you can't produce a signal that plays a role in telling the cell, or other cells to stop dividing, you'd expect to get uncontrolled tissue growth.
Great lecture.
The cancer data are mind-blowing
Psuedopagus is already reporting epigenetics to medicine and congenital ♥ diseases