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Fig. 3 | SpringerPlus

Fig. 3

From: Mechanism to control the cell lysis and the cell survival strategy in stationary phase under heat stress

Fig. 3

Functional model of rpoE-rseABC operon and role of σE in combating heat stress. The rseA gene product, RseA functions as an anti-sigma factor by binding to σE under normal condition. RseB also acts as a negative modulator and keep attached to RseA. Thus, the association of σE with RNA polymerase is hindered by formation of a tight complex between σE and RseA. Under stress condition, the YQF motif of the PDZ domain of the DegS protease senses the stress signal (usually through protein misfolding; i.e., the misfolded OMP precursor), RseB gets detached from RseA followed by the cleavage of C-terminus domain of RseA by DegS, and the further proteolytic cleavage of RseA by the metalloprotease YaeL results in the liberation of σE from RseA. The free σE binds to RNA polymerase which starts the transcription of the rpoE-rseABC operon genes required for response against stress signal

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