Determining regulators of SLC30A10 in mice using TagSeq
Determining regulators of SLC30A10 in mice using TagSeq
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Studies dating back to 1950's have shown that increased Mn intake also increases Mn excretion rate in mice. This homeostatic response to increased Mn exposure has been shown by our lab to be due to SLC30A10 upregulation by hypoxia-inducible factors. However, other regulators of SLC30A10 are yet unknown. In addition, SLC30A10 upregulation has been documented in either the liver or the small intestines, but not both organs, in different strains of mice.
In order to understand the overall change in the transcriptome in response to increased Mn intake, two strains of mice (C57BL/6 or 129S1) were treated with vehicle or 50mg/kg body weight Mn daily until 8 weeks of age. Samples collected from the midbrain, liver, and the intestines of the mice were used for TagSeq to determine differentially expressed genes-in addition to SLC30A10-as a response to increased Mn intake.
As expected, the strain-specific liver or intestine SLC30A10 upregulation was observed by TagSeq, along with a short list of other up- and downregulated genes.
None of the transcription factors from the ENCODE SCREEN list made it to the adjusted p value cutoff.
Therefore, these transcription factors were screened in the TagSeq dataset based on their unadjusted p values to determine potential transcription factors involved in Mn induced upregulation of SLC30A10.
Finally, we look at the "hits" from the ENCODE SCREEN data that are up- or downregulated along with upregulation of SLC30A10 in the liver of 129S Mice, and the intestines of C57 Mice:
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