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When E. coli undergoes cell division, the two daughter cells inherit the long-lived hok toxin from the parent cell. Due to the short half-life of the sok antitoxin, daughter cells inherit only small amounts and it quickly degrades.
If a daughter cell has inherited the R1 plasmid, it has inherited the sok gene and a strong promoter which brings about high levels of transcription. So much so that in an R1-positive cell, Sok transcript exists in considerable molar excess over Hok mRNA. Sok RNA then indirectly inhibits the translation of hok by inhibiting mok translation. There is a complementary region where sok transcript binds hok mRNA directly , but it does not occlude the Shine-Dalgarno sequence. Instead, sok RNA regulates the translation of the mok open reading frame, which nearly entirely overlaps that of hok. It is this translation-coupling which effectively allows sok RNA to repress the translation of hok mRNA.
The sok transcript forms a duplex with the leader region of hok mRNA and this is recognized by RNase III and degraded. The cleavage products are very unstable and soon decay.