According to new research, epigenetic regulation is required to ensure correct number of chromosomes in the daughter cells after division.
From ScienceDaily:
Normally when a cell divides, the chromosomes are segregated equally to two daughter cells. However, tumor cells frequently have either too few or too many chromosomes, leading to the incorrect expression of a number of genes. When a cell is about to divide, the cell division machinery takes hold of chromosomes by the centromere so that they may be pulled apart and one copy of each given to the daughter cells.
In the current study, researchers have shown that an epigenetic process, involving the attachment of a small protein to the histone H2B (called H2Bub1), facilitates an important structural change of the centromere immediately prior to cell division. It was previously shown that enzymes that modify histone H2B in this way also play a role in protecting against cancer. This was previously linked to defects in chromosomal repair.
Abstract Functional centromeres are essential for proper cell division. Centromeres are established largely by epigenetic processes resulting in incorporation of the histone H3 variant CENP-A. Here, we demonstrate the direct involvement of H2B monoubiquitination, mediated by RNF20 in humans or Brl1 in Schizosaccharomyces pombe, in centromeric chromatin maintenance. Monoubiquinated H2B (H2Bub1) is needed for this maintenance, promoting noncoding transcription, centromere integrity and accurate chromosomal segregation. A transient pulse of centromeric H2Bub1 leads to RNA polymerase II–mediated transcription of the centromere’s central domain, coupled to decreased H3 stability. H2Bub1-deficient cells have centromere cores that, despite their intact centromeric heterochromatin barriers, exhibit characteristics of heterochromatin, such as silencing histone modifications, reduced nucleosome turnover and reduced levels of transcription. In the H2Bub1-deficient cells, centromere functionality is hampered, thus resulting in unequal chromosome segregation. Therefore, centromeric H2Bub1 is essential for maintaining active centromeric chromatin. – Laia Sadeghi, Lee Siggens, J Peter Svensson, Karl Ekwall. Centromeric histone H2B monoubiquitination promotes noncoding transcription and chromatin integrity. Nature Structural & Molecular Biology, 2014; DOI: 10.1038/nsmb.2776
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“Could cancer sometimes be an outcome of failure?”
Of course. The whole organism is a multitude of carefully-controlled regulations. Indeed, it is probably very often the case, if not always, that diseases, including cancer, result from a breakdown in one of the regulations.
The reminds me of something I was thinking about just this morning — how people often talk about scientists discovering a “gene” for this or that disease. No, folks, there isn’t a “gene” for, say, heart disease. Yes, there are probably lots of genes that deal with heart function and are essential to it, but that means they are genes for heart function, not heart disease.
It would be like me saying I’ve discovered the part for my flat tire, and that the part is a tear in the tire wall. No, there isn’t a part for a flat tire; it is a failure of a part that results in a flat tire.
This should be clear to anyone who thinks about it long enough. Unfortunately, the lax wording and the fuzzy analysis that often accompanies evolutionary thinking can lead people to mistakenly think that a breakdown of a functional part is all just part of the evolutionary process, just as relevant as the construction of a wonderfully-functional new part. It is all just part of the same continuum of “change over time”, the thinking goes. It’s all just one big process of evolution.
This kind of muddled thinking is what leads to comments like wd400’s on the other thread, who referred to cancer as a form of evolution. OK, sure. If by “evolution” we mean a breakdown of normally functional systems, followed by disease and death.
But to the indoctrinated it is all just another example of “evolution” in action.
Peter Duesberg on “Aneuploidy and Cancer“: