Topic
Nuclear DNA
About: Nuclear DNA is a research topic. Over the lifetime, 3933 publications have been published within this topic receiving 185830 citations.
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TL;DR: In yeast, it is demonstrated that the rate of mtDNA fragments translocating to the nucleus increases during chronological aging, which may contribute to the chronological aging process by possibly increasing nuclear genomic instability in cells with advanced age.
Abstract: Migration of fragmented mitochondrial DNA (mtDNA) to the nucleus has been shown to occur in multiple species including yeast, plants, and mammals. Several human diseases, including Pallister-Hall syndrome and mucolipidosis, can be initiated by mtDNA insertion mutagenesis of nuclear DNA. In yeast, we demonstrated that the rate of mtDNA fragments translocating to the nucleus increases during chronological aging. The yeast chronological life span (CLS) is determined by the survival of non-dividing cell populations. Whereas yeast strains with elevated migration rates of mtDNA fragments to the nucleus showed accelerated chronological aging, strains with decreased mtDNA transfer rates to the nucleus exhibited an extended CLS. Although one of the most popular theories of aging is the free radical theory, migration of mtDNA fragments to the nucleus may also contribute to the chronological aging process by possibly increasing nuclear genomic instability in cells with advanced age.
50 citations
TL;DR: Covalent cross-linking of DNA to HMG I/Y by FR900482 in vivo is reported which represents the first example of a covalent DNA-drug-protein cross-link with a minor groove-binding oncoprotein and a potential novel mechanism through which these compounds exert their anti-tumor activity.
50 citations
TL;DR: It is concluded that past vicariant events associated with Pleistocene climate changes together with recent gene flow have created the observed intra‐specific cytonuclear discordance in Western North America.
Abstract: We investigated a major geographic break in mitochondrial DNA (mtDNA) haplotypes in deer mice, Peromyscus maniculatus, by analysing spatial variation in a 491-bp fragment of the mtDNA control region from 455 samples distributed across a north-south transect of 2000 km in Western North America. To determine whether the mtDNA break was reflected in the nuclear genome, we then compared spatial variation in 13 nuclear microsatellites of 95 individuals surrounding the mtDNA break. Using a canonical correlation analysis we found that nuclear genomic variation was not correlated with mtDNA differentiation. The contrasting patterns of variation in mtDNA and nuclear DNA are consistent with a hypothesis of historic genetic drift that occurred in isolated refugia combined with recent gene flow between the formerly isolated refugial populations. A Mantel test of genetic vs. geographic distance revealed that recent gene flow between deer mouse populations has been high. We conclude that past vicariant events associated with Pleistocene climate changes together with recent gene flow have created the observed intra-specific cytonuclear discordance in Western North America.
50 citations
TL;DR: Thirty-one clover species with significant agronomic value, originating from Eurasia, Africa and America, were analyzed to reveal their nuclear DNA content and propidium iodide/4,6-diamidino-2-phenylindole (PI/DAPI) ratio and polyploidy provided the most informative measure of interspecific DNA content variation.
50 citations
TL;DR: Experimental data support the idea that by modulating these repair mechanisms, greater killing effect to anticancer agents would occur, and several of these key DNA repair proteins which are actively under investigation as novel sites for intervention in cancer biology are discussed.
Abstract: The DNA repair process in mammalian cells is a multi-pathway mechanism that protects cells from the plethora of DNA damaging agents that are known to attack nuclear DNA. Moreover, the majority of current anticancer therapies (e.g. ionising radiation and chemotoxic therapies) rely on this ability to create DNA lesions, leading to apoptosis/cell death. A cells natural ability to repair such DNA damage is a major cause of resistance to these existing antitumour agents. It seems logical, therefore, that by modulating these repair mechanisms, greater killing effect to anticancer agents would occur. Experimental data support this, either through knockout studies or by the use of pharmacological inhibitors which target some of the key regulatory proteins involved in the DNA repair process. Several of these key DNA repair proteins which are actively under investigation as novel sites for intervention in cancer biology are discussed.
50 citations