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DNA damaging agent doxorubicin induces the expression of myotonic dystrophy kinase protein in tumor suppressor p53 dependent manner

ABSTRACT: Tumor suppressor p53 plays an integral role in DNA damage-induced apoptosis, which is one of the biological processes to protect against tumor progression. Cell shape is dramatically changed undergoing apoptosis, which is often associated with actomyosin contraction; however, it remains entirely elusive how p53 regulates actomyosin contraction in response to DNA-damaging agent. We here show that p53 controls expression of myotonic dystrophy protein kinase (DMPK), which is known to upregulate actomyosin contraction. To identify a novel p53 regulating gene encoding the modulator of myosin, we performed a DNA microarray and then found that, in response to DNA-damaging agent doxorubicin, DMPK expression was increased in a p53-dependent manner.

ORGANISM(S): Mus musculus

PROVIDER: GSE134201 | GEO | 2019/09/05

REPOSITORIES: GEO

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Project description:We have looked at the transcriptional response of well characterised Synechococcus open ocean (WH8102) and coastal (CC9311) isolates to two DNA damaging agents, mitomycin C and ethidium bromide, using whole genome expression microarrays. The coastal strain, which was able to grow on higher concentrations of both chemicals, showed differential regulation of a larger proportion of its genome following M-bM-^@M-^Xtoxic shockM-bM-^@M-^Y treatment with each agent. Many of the orthologous genes in these strains, including those encoding sensor kinases, showed different transcriptional responses, with the CC9311 genes more likely to show significant changes for each tested treatment. While the overall response of each strain was considerably different, there were distinct transcriptional responses common to both strains observed for each DNA damaging agent, linked to the mode of action of each chemical. In both CC9311 and WH8102 there was evidence of SOS response induction under mitomycin C treatment, with genes encoding recA, the lexA repressor and umuC significantly upregulated in this experiment but not under ethidium bromide treatment. Conversely, ethidium bromide treatment tended to result in upregulation of the DNA-directed RNA polymerase genes, not observed following mitomycin C treatment. Interestingly, a large number of genes residing on putative genomic island regions of each genome also showed significant upregulation under one or both chemical treatments. In this series four conditions have been analyzed. These are 2 hour incubations (shock treatment) with ethidium bromide (EB, final conc 2ug/mL) and mitomycin C (MC, final conc 0.5 ug/mL) for Synechococcus sp. WH8102 and CC9311. For each slide, an experimental RNA sample was labeled with Cy3 or Cy5 and was hybridized with a reference RNA from a control sample (no addition of chemical agent) labeled with the other Cy dye. There are six slides per condition, each with at least two biological replicates and three technical replicates, including at least one flip-dye comparison. Each slide contains six replicate spots per gene.

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DNA damaging agent doxorubicin induces the expression of myotonic dystrophy kinase protein in tumor suppressor p53 dependent manner

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