The obligate intracellular bacterial pathogen has a unique developmental cycle consisting of two contrasting cellular forms. Whereas the primary sigma factor, σ, is involved in the expression of the majority of chlamydial genes throughout the developmental cycle, expression of several late genes requires the alternative sigma factor σ In prior work, we identified GrgA as a specific transcription factor that activates σ-dependent transcription by binding DNA and interacting with a non-conserved region (NCR) of σ Here, we extend these findings by showing GrgA can also activate σ-dependent transcription through direct interaction with σ We measure the binding affinity of GrgA for both σ and σ, and we identify regions of GrgA important for σ-dependent transcription. Similar to results obtained with σ, we find that GrgA's interaction with σ involves a NCR located upstream of conserved region 2 of σ Our findings suggest GrgA is an important regulator of both σ- and σ-dependent transcription in and further highlight NCRs of bacterial RNA polymerase as targets for regulatory factors unique to particular organisms. is the number one sexually transmitted bacterial pathogen worldwide. A substantial proportion of -infected women develop infertility, pelvic inflammatory syndrome and other serious complications. is also a leading infectious cause of blindness in under-developed countries. The pathogen has a unique developmental cycle, which is transcriptionally regulated. The discovery of an expanded role for the specific transcription factor GrgA helps understand progression of the chlamydial developmental cycle.
The sexually transmitted obligate intracellular bacterial pathogen Chlamydia trachomatis has a unique developmental cycle consisting of two contrasting cellular forms. Whereas the primary Chlamydia sigma factor, σ66, is involved in the expression of the majority of chlamydial genes throughout the developmental cycle, expression of several late genes requires the alternative sigma factor σ28. In prior work we identified GrgA as a Chlamydia-specific transcription factor that activates σ66-dependent transcription by binding DNA and interacting with a non-conserved region (NCR) of σ66. Here, we extend these findings by showing GrgA can also activate σ28-dependent transcription through direct interaction with σ28. We measure the binding affinity of GrgA for both σ66and σ28, and we identify regions of GrgA important for σ28-dependent transcription. Similar to results obtained with σ66, we find that GrgA’s interaction with σ28 involves a NCR located upstream of conserved region 2 of σ28. Our findings suggest GrgA is an important regulator of both σ66- and σ28-dependent transcription in C. trachomatis and further highlight NCRs of bacterial RNA polymerase as targets for regulatory factors unique to particular organisms.
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