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Mutator transposon activation after UV-B involves chromatin remodeling.

ABSTRACT: Spontaneous silencing of MuDR/Mu transposons occurs in approximately 10-100% of the progeny of an active plant, and once silenced reactivation is very rare. To date, only radiation treatments have reactivated silenced Mu; for example UV-B radiation reactivated Mutator activities. Here we have investigated possible mechanisms by which UV-B could reactivate Mu transposons by monitoring transcript abundance, epigenetic DNA marks, and chromatin factors associated with these elements. We demonstrate that both mudrA and B transcripts are expressed at higher levels after an 8 h-UV-B treatment, in both active Mutator and silencing plants, and that different chromatin remodeling events occur in the promoter regions of MuDR than in non-autonomous Mu1 elements. Increased transcript abundance is accompanied by an increase in histone H3 acetylation and by decreased DNA and H3K9me2 methylation. No changes in siRNA levels were detected. In contrast, the decrease in H3K9me2 present at Mu elements after UV-B is significant in silencing plants, suggesting that early changes in H3 methylation in K9, chromatin remodeling, and transcription factor binding contribute directly to transposon reactivation by UV-B in maize.

SUBMITTER: Questa JI

PROVIDER: S-EPMC2911508 | biostudies-literature | 2010 May

REPOSITORIES: biostudies-literature

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Mutator transposon activation after UV-B involves chromatin remodeling.

Qüesta Julia I JI Walbot Virginia V Casati Paula P

Epigenetics 20100510 4

Spontaneous silencing of MuDR/Mu transposons occurs in approximately 10-100% of the progeny of an active plant, and once silenced reactivation is very rare. To date, only radiation treatments have reactivated silenced Mu; for example UV-B radiation reactivated Mutator activities. Here we have investigated possible mechanisms by which UV-B could reactivate Mu transposons by monitoring transcript abundance, epigenetic DNA marks, and chromatin factors associated with these elements. We demonstrate ...[more]

PMID: 20421734

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Project description:Following brain injury or in neurodegenerative diseases, astrocytes become reactive and may suffer pathological remodeling, features of which are the loss of their homeostatic functions and a pro-inflammatory gain of function that facilitates neurodegeneration. Pharmacological intervention to modulate this astroglial response and neuroinflammation is an interesting new therapeutic research strategy, but it still requires a deeper understanding of the underlying cellular and molecular mechanisms of the phenomenon. Based on the known microglial-astroglial interaction, the prominent role of the nuclear factor kappa B (NF-κB) pathway in mediating astroglial pathological pro-inflammatory gain of function, and its ability to recruit chromatin-remodeling enzymes, we first explored the microglial role in the initiation of astroglial pro-inflammatory conversion and then monitored the progression of epigenetic changes in the astrocytic chromatin. Different configurations of primary glial culture were used to modulate microglia-astrocyte crosstalk while inducing pro-inflammatory gain of function by lipopolysaccharide (LPS) exposure. In vivo, brain ischemia by cortical devascularization (pial disruption) was performed to verify the presence of epigenetic marks in reactive astrocytes. Our results showed that 1) microglia is required to initiate the pathological conversion of astrocytes by triggering the NF-κB signaling pathway; 2) this interaction is mediated by soluble factors and induces stable astroglial phenotypic changes; 3) the pathological conversion promotes chromatin remodeling with stable increase in H3K9K14ac, temporary increase in H3K27ac, and temporary reduction in heterochromatin mark H3K9me3; and 4) in vivo reactive astrocytes show increased H3K27ac mark in the neuroinflammatory milieu from the ischemic penumbra. Our findings indicate that astroglial pathological pro-inflammatory gain of function is associated with profound changes in the configuration of astrocytic chromatin, which in turn are initiated by microglia-derived cues. These results open a new avenue in the study of potential pharmacological interventions that modify the initiation and stabilization of astroglial pathological remodeling, which would be useful in acute and chronic CNS injury. Epigenetic changes represent a plausible pharmacological target to interfere with the stabilization of the pathological astroglial phenotype.

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Mutator transposon activation after UV-B involves chromatin remodeling.

Publications

Mutator transposon activation after UV-B involves chromatin remodeling.

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