A heat-induced HagF-HrcA regulatory loop promotes chlamydial fitness and infectious progeny yield under stress.

HagF antagonizes the heat-inducible repressor HrcA in Chlamydia, and this HagF–HrcA loop boosts infectious elementary body yield under heat stress.

• Why it matters: Stress survival depends on protein homeostasis, but streamlined genomes make the regulatory logic unclear, especially how heat-responsive transcription is coordinated with development.
• What they did: The study used genetic and biochemical tests, including HagF overexpression and CRISPRi knockdown, to show HrcA represses hagF and five targets under non-stress, while heat induces HagF that binds HrcA.
• The result: Heat-driven HagF induction attenuates HrcA repression, enhancing chaperone gene induction—especially from the hrcA-grpE-dnaK operon—and increasing infectious elementary body yield under restrictive conditions.

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