mitochondrial dna viral degradation

Breaks in mtDNA that occur through other means such as treatment with toxic DNA-damaging agents or errors in replication often lead to compromised organelle function 9But Tigano and colleagues. EpsteinBarr virus immediate-early protein Zta co-opts mitochondrial single-stranded DNA binding protein to promote viral and inhibit mitochondrial DNA replication.

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We show that an amino-terminally truncated UL12 isoform-UL125-localizes to mitochondria and triggers mitochondrial DNA depletion in the absence of other HSV gene products.

. By manipulating mitochondrial dynamics 1 ssRNA viruses either directly or indirectly manipulate a number of cellular processes to promote viral replication and immune evasion. Mechanistically the HSV1 virus encodes a nuclease UL125 which localises to the mitochondria and degrades mtDNA resulting in complete loss of mtDNA in infected cells 40 41. Here we show that the ubiquitous human pathogen herpes simplex virus HSV induces rapid and complete degradation of host mitochondrial DNA during productive infection of cultured mammalian cells.

We recently reported that mitochondria-derived cytoplasmic double-stranded DNA dsDNA that has escaped lysosomal degradation induces. An early report pointing to the existence of degradation of damaged mtDNA by Suter and Richter showed that fragmented mtDNA contains a 15-fold higher level of 8-oxodG than the intact circular mtDNA in rat liver mitochondria which suggested that an efficient mtDNA repair or degrading system exists in mitochondria. The presence of ectopic DNA in the cytoplasm induces inflammation and cell death.

The depletion of mitochondrial DNA requires the viral UL12 gene which encodes a conserved nuclease with orthologues in all herpesviruses. Data from experimental animals also support the notion that. The depletion of mitochondrial DNA requires the viral UL12 gene which encodes a conserved nuclease with orthologues in all herpesviruses.

Mitochondria harbor their own genomic DNA which encodes protein subunits of the. It has been widely reported that leakage of nuclear DNA into the cytoplasm can mainly be sensed by cyclic GMP-AMP synthase cGAS. Here we document that persistent mitochondria DNA mtDNA damage due to mitochondrial overexpression of the Y147A mutant uracil-N-glycosylase as well as mitochondrial overexpression of bacterial Exonuclease III or Herpes Simplex Virus protein UL125M185 can induce a complete loss of mtDNA ρ0 phenotype without compromising the viability of cells.

Mitochondria play a central role in bioenergetics and fulfill a plethora of functions in cell signaling programmed cell death and biosynthesis of key protein cofactors. Removal of mtDNA in infected cells does not appear to impact HSV replication 42. A quality control measure for mitochondrial genome maintenance and stress response.

These include increasing mitochondrial activity 2 inhibiting MAVS activation 3 and activating mitophagy 4 to prevent apoptosis 5. We show that an.

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