Premium
Origin of diplochromosomal polyploidy in near‐senescent fibroblast cultures: Heterochromatin, telomeres and chromosomal instability (CIN)
Author(s) -
Walen Kirsten H.
Publication year - 2007
Publication title -
cell biology international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.932
H-Index - 77
eISSN - 1095-8355
pISSN - 1065-6995
DOI - 10.1016/j.cellbi.2007.06.015
Subject(s) - heterochromatin , biology , telomere , chromosome instability , mitosis , chromatin , genome instability , centromere , microbiology and biotechnology , genetics , anaphase , epigenetics , chromosome , chromosome segregation , cell cycle , dna damage , dna , cell , gene
The near‐senescence associated phenomena of increases in cells with chromosomal damage (CIN) and in endopolyploid mitotic cells were analyzed for possible inter‐relationships by cytogenetics. Gross chromosomal abnormalities in all phases of mitosis were analyzed in situ. Hetrochromatization of telomeres, centromeres and interstitial chromatin regions (i.e., chromocenters/SAHF) were shown to be specific occurrences in the near‐senescent phase. Stickiness between such chromatin regions caused breakage/fragmentation by anaphase‐pulls on clumped chromosomes. Gluey heterochromatin is therefore, seen as a cause of CIN in near‐senescence. Detrimental effects on chromosomes from heterochromatin have been observed for decades, and can be explained from chromatin remodeling in epigenetics. A consequence of genomic damage was re‐replication to polyploidy of arrest‐escaped cells with G2/M‐DNA content. This second synthetic period produced diplochromosomal cells that cycled by bi‐polar division into genome reduced cells. This sequence from h‐chromatization to CIN and further to cycling endopolyploidy is believed to be a basic mechanism for the production of genetic variability in neoplasia.