Entering the post-epigenomic age: back to epigenetics
It is undeniably one of the greatest findings in biology that (with some very minor exceptions) every cell in the body possesses the whole genetic information needed to generate a complete individual. Today, this concept has been so thoroughly assimilated that we struggle to still see how surprising...
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2018-03-01
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Online Access: | https://royalsocietypublishing.org/doi/pdf/10.1098/rsob.180013 |
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doaj-f0468123db6f499c8285d1eae0b409c52020-11-25T03:57:02ZengThe Royal SocietyOpen Biology2046-24412018-03-018310.1098/rsob.180013180013Entering the post-epigenomic age: back to epigeneticsSebastian BultmannStefan H. StrickerIt is undeniably one of the greatest findings in biology that (with some very minor exceptions) every cell in the body possesses the whole genetic information needed to generate a complete individual. Today, this concept has been so thoroughly assimilated that we struggle to still see how surprising this finding actually was: all cellular phenotypes naturally occurring in one person are generated from genetic uniformity, and thus are per definition epigenetic. Transcriptional mechanisms are clearly critical for developing and protecting cell identities, because a mis-expression of few or even single genes can efficiently induce inappropriate cellular programmes. However, how transcriptional activities are molecularly controlled and which of the many known epigenomic features have causal roles remains unclear. Today, clarification of this issue is more pressing than ever because profiling efforts and epigenome-wide association studies (EWAS) continuously provide comprehensive datasets depicting epigenomic differences between tissues and disease states. In this commentary, we propagate the idea of a widespread follow-up use of epigenome editing technology in EWAS studies. This would enable them to address the questions of which features, where in the genome, and which circumstances are essential to shape development and trigger disease states.https://royalsocietypublishing.org/doi/pdf/10.1098/rsob.180013crisprepigenome-wide association studiesepigenome editingcas9epigenomicsdcas9 |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Sebastian Bultmann Stefan H. Stricker |
spellingShingle |
Sebastian Bultmann Stefan H. Stricker Entering the post-epigenomic age: back to epigenetics Open Biology crispr epigenome-wide association studies epigenome editing cas9 epigenomics dcas9 |
author_facet |
Sebastian Bultmann Stefan H. Stricker |
author_sort |
Sebastian Bultmann |
title |
Entering the post-epigenomic age: back to epigenetics |
title_short |
Entering the post-epigenomic age: back to epigenetics |
title_full |
Entering the post-epigenomic age: back to epigenetics |
title_fullStr |
Entering the post-epigenomic age: back to epigenetics |
title_full_unstemmed |
Entering the post-epigenomic age: back to epigenetics |
title_sort |
entering the post-epigenomic age: back to epigenetics |
publisher |
The Royal Society |
series |
Open Biology |
issn |
2046-2441 |
publishDate |
2018-03-01 |
description |
It is undeniably one of the greatest findings in biology that (with some very minor exceptions) every cell in the body possesses the whole genetic information needed to generate a complete individual. Today, this concept has been so thoroughly assimilated that we struggle to still see how surprising this finding actually was: all cellular phenotypes naturally occurring in one person are generated from genetic uniformity, and thus are per definition epigenetic. Transcriptional mechanisms are clearly critical for developing and protecting cell identities, because a mis-expression of few or even single genes can efficiently induce inappropriate cellular programmes. However, how transcriptional activities are molecularly controlled and which of the many known epigenomic features have causal roles remains unclear. Today, clarification of this issue is more pressing than ever because profiling efforts and epigenome-wide association studies (EWAS) continuously provide comprehensive datasets depicting epigenomic differences between tissues and disease states. In this commentary, we propagate the idea of a widespread follow-up use of epigenome editing technology in EWAS studies. This would enable them to address the questions of which features, where in the genome, and which circumstances are essential to shape development and trigger disease states. |
topic |
crispr epigenome-wide association studies epigenome editing cas9 epigenomics dcas9 |
url |
https://royalsocietypublishing.org/doi/pdf/10.1098/rsob.180013 |
work_keys_str_mv |
AT sebastianbultmann enteringthepostepigenomicagebacktoepigenetics AT stefanhstricker enteringthepostepigenomicagebacktoepigenetics |
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