In a mammalian cell for a reason “A” – viral infection, environmental pressure, stress, etc., - occurs an asymmetric cell division (ACD) at M-phase for a factor “B” or a complex “C”. If, this factor or complex is present in one of the two daughter cells for next generations – the phenomenon could be a Genetic or Epigenetic event? Could be consider that the reason “A” affects genetic inheritance?
Asymmetric cell division or unequal distribution of a protein during cell division is by itself neither genetic nor epigenetic. Unless the trait is now heritable for subsequent generations of cell division, it is not considered epigenetic. If the trait is heritable, I would call it epigenetic if the stress altered the histone or DNA methylation patterns in a heritable manner. If the stress altered the DNA sequences, such as a retroviral insertion, it would be a genetic effect.
Asymmetric cell division or unequal distribution of a protein during cell division is by itself neither genetic nor epigenetic. Unless the trait is now heritable for subsequent generations of cell division, it is not considered epigenetic. If the trait is heritable, I would call it epigenetic if the stress altered the histone or DNA methylation patterns in a heritable manner. If the stress altered the DNA sequences, such as a retroviral insertion, it would be a genetic effect.
Short but correct answer in my opinion. In husbandry animals this subject is very important, and should be more investigated, considering poor environmental conditions.
The bacteria´s adaptative mutation, in a diferente way is na interesting subject.
Congratulations for the question.
Ill ask this question out of interest and "ignorance". Say one had some DNA (and control DNA naturally) which may have an epigenetic modification. What does one do. Fine to say look at methylation and/or histone modification but how does one do that. Can it be done on a "global" scale or does one need a list of genes which are differentially expressed.
Peter, for DNA methylation one can look at the entire genome or specific genes. Bisulfite conversion coupled to next gen sequencing can be used to get the DNA methylome for an entire genome. For whole genome histone modifications, you need to isolate chromatin and use antibodies against the specific modifications to immunoprecipitate the fragmented chromatin. The DNA is then purified and sequenced and compared to input or the reference genome to look for peaks of enrichment (ChIP-Seq method), This can also be done more easily for specific genes using PCR primer pairs for your region.
As I have initially introduced in this question, ChoroEpigenetics might represent a new discipline in modern Biology and a new model of cell-cell communication and Epigenetics transmission and inheritance. This could have an important effect in anticancer and anti-viral strategies. Despite difficulties of an independent research activity that I am pursuing, the concrete scientific data will be presented in the near future in support of this model.
Meanwhile an extraordinary information coming from Alzheimer’s disease suggests that information encoded in a non DNA/RNA context can be transmitted form one cell generation to another.
Nature 09 September 2015; “Only a decade ago, the idea that Alzheimer’s disease might be transmissible between people would have been laughed off the stage. But scientists have since shown that tissues can transmit symptoms of the disease between animals — and new results imply that humans, at least in one unusual circumstance, may not be an exception.
The findings, published in this issue of Nature, emerged during autopsy studies of the brains of eight people who had died of the rare but deadly Creutzfeldt–Jakob disease (CJD; Z. Jaunmuktane et al. Nature 525, 247–250; 2015). They contracted it decades after treatment with contaminated batches of growth hormone that had been extracted from the pituitary glands of human cadavers. Six of the brains, in addition to the damage caused by CJD, harboured the tell-tale amyloid pathology that is associated with Alzheimer’s disease.
“This is the first evidence of real-world transmission of amyloid pathology,” says molecular neuroscientist John Hardy of University College London (UCL). “It is potentially concerning.”
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