Patho-epigenetics of disease

J. Mináróvits, Hans Helmut Niller

Research output: Book/ReportBook

Abstract

In multicellular organisms the establishment, maintenance, and programmed alterations of cell-type specific gene expression patterns are regulated by epigenetic mechanisms. Thus, epigenetic alterations (DNA methylation, DNA associated Polycomb-Trithorax protein complexes, histone modifications) ensure the unique transcriptional activity and phenotypic diversity of diploid cells that carry identical or nearly identical DNA sequences.Because DNA methyltransferase I (DNMT1) associates with replication foci during S phase and prefers hemimethylated DNA as a substrate, DNMT1 ensures the clonal propagation of cytosine methylation patterns (maintenance methylation). Thus, DNA methylation may provide a memory function by helping progeny cells to "remember" their proper cellular identity.An alternative system of epigenetic memory, the Polycomb and Trithorax groups of protein complexes, that may operate both independently from and in concert with DNA methylation, ensures the heritable regulation of gene expression viamodification of histone tails.The complex interplay of epigenetic regulatory mechanisms permits both the dynamic modulation of gene expression and the faithful transmission of gene expression patterns to each progeny cell upon division. These carefully orchestrated processes can go wrong, however, resulting in epigenetic reprogramming of the cells that may manifest in pathological changes, as it was first realized during the studies of epigenetic alterations in malignant tumors. By now it became a well established fact that not only genetic changes, but also the disruption of epigenetic regulation can result in carcinogenesis and tumor progression. Scientists working in other fields soon followed the pioneering work of cancer researchers, and revealed that epigenetic dysregulation forms the basis of a wide spectrum of human diseases.

Original languageEnglish
PublisherSpringer New York
Number of pages465
ISBN (Print)9781461433453, 1461433444, 9781461433446
DOIs
Publication statusPublished - Sep 1 2014

Fingerprint

Epigenomics
DNA Methylation
Gene Expression
Methylation
DNA
Histone Code
Polycomb-Group Proteins
Maintenance
Neoplasms
Cytosine
Methyltransferases
Gene Expression Regulation
Diploidy
S Phase
Cell Division
Histones
Tail
Carcinogenesis
Research Personnel
Proteins

ASJC Scopus subject areas

  • Medicine(all)
  • Immunology and Microbiology(all)

Cite this

Patho-epigenetics of disease. / Mináróvits, J.; Niller, Hans Helmut.

Springer New York, 2014. 465 p.

Research output: Book/ReportBook

Mináróvits, J. ; Niller, Hans Helmut. / Patho-epigenetics of disease. Springer New York, 2014. 465 p.
@book{5b5b05a62f594f4c82e7f4286dfbe076,
title = "Patho-epigenetics of disease",
abstract = "In multicellular organisms the establishment, maintenance, and programmed alterations of cell-type specific gene expression patterns are regulated by epigenetic mechanisms. Thus, epigenetic alterations (DNA methylation, DNA associated Polycomb-Trithorax protein complexes, histone modifications) ensure the unique transcriptional activity and phenotypic diversity of diploid cells that carry identical or nearly identical DNA sequences.Because DNA methyltransferase I (DNMT1) associates with replication foci during S phase and prefers hemimethylated DNA as a substrate, DNMT1 ensures the clonal propagation of cytosine methylation patterns (maintenance methylation). Thus, DNA methylation may provide a memory function by helping progeny cells to {"}remember{"} their proper cellular identity.An alternative system of epigenetic memory, the Polycomb and Trithorax groups of protein complexes, that may operate both independently from and in concert with DNA methylation, ensures the heritable regulation of gene expression viamodification of histone tails.The complex interplay of epigenetic regulatory mechanisms permits both the dynamic modulation of gene expression and the faithful transmission of gene expression patterns to each progeny cell upon division. These carefully orchestrated processes can go wrong, however, resulting in epigenetic reprogramming of the cells that may manifest in pathological changes, as it was first realized during the studies of epigenetic alterations in malignant tumors. By now it became a well established fact that not only genetic changes, but also the disruption of epigenetic regulation can result in carcinogenesis and tumor progression. Scientists working in other fields soon followed the pioneering work of cancer researchers, and revealed that epigenetic dysregulation forms the basis of a wide spectrum of human diseases.",
author = "J. Min{\'a}r{\'o}vits and Niller, {Hans Helmut}",
year = "2014",
month = "9",
day = "1",
doi = "10.1007/978-1-4614-3345-3",
language = "English",
isbn = "9781461433453",
publisher = "Springer New York",

}

TY - BOOK

T1 - Patho-epigenetics of disease

AU - Mináróvits, J.

AU - Niller, Hans Helmut

PY - 2014/9/1

Y1 - 2014/9/1

N2 - In multicellular organisms the establishment, maintenance, and programmed alterations of cell-type specific gene expression patterns are regulated by epigenetic mechanisms. Thus, epigenetic alterations (DNA methylation, DNA associated Polycomb-Trithorax protein complexes, histone modifications) ensure the unique transcriptional activity and phenotypic diversity of diploid cells that carry identical or nearly identical DNA sequences.Because DNA methyltransferase I (DNMT1) associates with replication foci during S phase and prefers hemimethylated DNA as a substrate, DNMT1 ensures the clonal propagation of cytosine methylation patterns (maintenance methylation). Thus, DNA methylation may provide a memory function by helping progeny cells to "remember" their proper cellular identity.An alternative system of epigenetic memory, the Polycomb and Trithorax groups of protein complexes, that may operate both independently from and in concert with DNA methylation, ensures the heritable regulation of gene expression viamodification of histone tails.The complex interplay of epigenetic regulatory mechanisms permits both the dynamic modulation of gene expression and the faithful transmission of gene expression patterns to each progeny cell upon division. These carefully orchestrated processes can go wrong, however, resulting in epigenetic reprogramming of the cells that may manifest in pathological changes, as it was first realized during the studies of epigenetic alterations in malignant tumors. By now it became a well established fact that not only genetic changes, but also the disruption of epigenetic regulation can result in carcinogenesis and tumor progression. Scientists working in other fields soon followed the pioneering work of cancer researchers, and revealed that epigenetic dysregulation forms the basis of a wide spectrum of human diseases.

AB - In multicellular organisms the establishment, maintenance, and programmed alterations of cell-type specific gene expression patterns are regulated by epigenetic mechanisms. Thus, epigenetic alterations (DNA methylation, DNA associated Polycomb-Trithorax protein complexes, histone modifications) ensure the unique transcriptional activity and phenotypic diversity of diploid cells that carry identical or nearly identical DNA sequences.Because DNA methyltransferase I (DNMT1) associates with replication foci during S phase and prefers hemimethylated DNA as a substrate, DNMT1 ensures the clonal propagation of cytosine methylation patterns (maintenance methylation). Thus, DNA methylation may provide a memory function by helping progeny cells to "remember" their proper cellular identity.An alternative system of epigenetic memory, the Polycomb and Trithorax groups of protein complexes, that may operate both independently from and in concert with DNA methylation, ensures the heritable regulation of gene expression viamodification of histone tails.The complex interplay of epigenetic regulatory mechanisms permits both the dynamic modulation of gene expression and the faithful transmission of gene expression patterns to each progeny cell upon division. These carefully orchestrated processes can go wrong, however, resulting in epigenetic reprogramming of the cells that may manifest in pathological changes, as it was first realized during the studies of epigenetic alterations in malignant tumors. By now it became a well established fact that not only genetic changes, but also the disruption of epigenetic regulation can result in carcinogenesis and tumor progression. Scientists working in other fields soon followed the pioneering work of cancer researchers, and revealed that epigenetic dysregulation forms the basis of a wide spectrum of human diseases.

UR - http://www.scopus.com/inward/record.url?scp=84929524486&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84929524486&partnerID=8YFLogxK

U2 - 10.1007/978-1-4614-3345-3

DO - 10.1007/978-1-4614-3345-3

M3 - Book

SN - 9781461433453

SN - 1461433444

SN - 9781461433446

BT - Patho-epigenetics of disease

PB - Springer New York

ER -