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 (
pictured), 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. Daughter cells without a copy of the R1 plasmid
die because they do not have the means to produce more
sok antitoxin transcript to inhibit translation of the inherited
hok mRNA. The killing system is said to be postsegregational (PSK), since cell death occurs after
segregation of the plasmid. ==Hok toxin==