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Abstract

While many bacteria divide by symmetric binary fission, some
alphaproteobacteria have strikingly asymmetric cell cycles, producing
offspring that differs significantly in their morphology and
reproductive state. To establish this asymmetry, these species employ a
complex cell cycle regulatory pathway based on two-component signaling
cascades. At the center of this network is the essential DNA-binding
response regulator CtrA, which acts as a transcription factor
controlling numerous genes with cell cycle-relevant functions as well as
a regulator of chromosome replication. The DNA-binding activity of CtrA
is controlled at the level of both protein phosphorylation and
stability, dependent on an intricate network of regulatory proteins,
whose function is tightly coordinated in time and space. CtrA is
differentially activated in the two (developing) offspring, thereby
establishing distinct transcriptional programs that ultimately determine
their distinct cell fates. Phase-separated polar microdomains of
changing composition sequester proteins involved in the (in-)activation
and degradation of CtrA specifically at each pole. In this review, we
summarize the current knowledge of the CtrA pathway and discuss how it
has evolved to regulate the cell cycle of morphologically distinct
alphaproteobacteria.