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JUMPING GENES. “However, in response to a potential decay of the chromatin structure during aging, excess retrotransposon transcription prevents recruitment of cohesion and condensin, causing persistent DNA damage checkpoint activation and senescence.” http://journal.frontiersin.org/article/10.3389/fgene.2013.00136/full View in LinkedIn

SO ENDS this first of two weekends on plant alternation of generations. That such a complex system exists is in part due to the necessity of not increasing chromosome numbers during successive generations, as well as the cobbling together of available tools that were handy. Evolution is a zig zaggy chaotic process with many dead ends and mistakes. Nothing was purpose-built. View in LinkedIn

BACK TO CHROMATIN. “Telomere-mediated activation of the DNA damage response appears to be intimately linked to the chromatin structure. Specifically, it was shown that chronic DNA damage from the processed telomeres also affects histone expression leading to their depletion and to the depletion of the central histone chaperones.” http://journal.frontiersin.org/article/10.3389/fgene.2013.00136/full View in LinkedIn

DIFFERENT HELPER CELL GROUPS. "Depending on their sex and their stage of development, plant reproductive cell lineages are associated with different supporting cell populations. In the stamen, male meiotic cells are invested by a layer of sporophytic (somatic) tapetal cells, which are essential for postmeiotic development and, particularly, the synthesis of the sporopollenin pollen wall and its coating." http://www.sciencedirect.com/science/article/pii/S1534580713000427 View in LinkedIn

TELOMERES AND DNA DAMAGE. “Telomere length is highly connected with the replicative lifespan of metazoan cells. Telomeres shorten with each successive round of DNA replication until one telomere reaches a threshold of “shortness” that emits a chronic DNA damage signal that causes the cell to cease dividing and enter senescence. Mechanistically, the short telomeres are seen as chronic DNA damage by the cell, resulting in the activation of the DNA damage response, which causes a G1 cell cycle arrest.” http://journal.frontiersin.org/article/10.3389/fgene.2013.00136/full View in LinkedIn

OUTSOURCED FUNCTIONS. "It is also evident that certain functions vital for protecting transgenerational genome integrity in animal germ cells, such as the suppression of transposition in the germ cell genome, has been partially “outsourced” to gametophytic helper cells in plants." (Targeted at suppressing parasitic mobile genetic elements by transposing silencing). http://www.sciencedirect.com/science/article/pii/S1534580713000427 View in LinkedIn

HUMAN ALU REPEAT. “Over 5% of the mammalian genome consists of short interspersed elements (SINEs), typified by the human Alu repeat. These are RNA polymerase III transcribed sequences whose expression is usually silenced. However, upon prolonged exposure to DNA damaging agents that predominantly cause double strand breaks, transcription from the human Alu elements and murine SINEs is strongly induced.” http://journal.frontiersin.org/article/10.3389/fgene.2013.00136/full View in LinkedIn

DNA DAMAGE RESPONSE. “Several different types of non-coding RNAs have been implicated in the DNA damage response. For example, many microRNAs (miRNAs) regulate genes that are involved in the DNA damage response." http://journal.frontiersin.org/article/10.3389/fgene.2013.00136/full View in LinkedIn

IMPORTANT REVIEW. “Here we will discuss how non-coding RNAs contribute to the relationships among chromatin structure, genomic integrity, and cellular senescence." http://journal.frontiersin.org/article/10.3389/fgene.2013.00136/full View in LinkedIn

CHROMATIN. “Given the critical role of chromatin in regulating genomic stability and gene expression, it is tempting to speculate that some of the changes in gene expression and genomic integrity that occur during aging may be caused by the global changes to the chromatin structure that accompany aging.” http://journal.frontiersin.org/article/10.3389/fgene.2013.00136/full View in LinkedIn