Kidney derived MDCK cells are protected from the stress of hypertonicity by accumulating compatible osmolytes. Accumulation of the compatible osmolytes myo-inositol and betaine is driven by hypertonicity-induced stimulation of transcription of the genes coding for the myo-inositol cotransporter and the betaine cotransporter. We tested the importance of the mitogen-activated protein kinase pathway in transcriptional activation of the genes for the two osmolytes cotransporters because this kinase pathway is rapidly activated when cells are exposed to hypertonicity and a mitogen-activated protein kinase pathway is essential for the osmo-protective transcriptional response of yeast to hypertonicity. Eliminating the activation of mitogen-activated protein kinase did not block the hypertonicity induced increase in accumulation of osmolyte transporter mRNA.
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