One of the most prevalent sexually transmitted diseases is caused by the bacterium Chlamydia trachomatis and leads to blindness if left untreated. Upon infection, metabolically inert cells differentiate, through gene expression, to become metabolically active cells that divide by binary fission. It has been proposed that release from the inert state is dependent on heat-shock proteins that both activate the reproductive cycle and facilitate the binding of chlamydiae to host cells. Researchers made the following observations regarding the heat-shock regulatory system in Chlamydia trachomatis: (1) a regulator protein (call it R) binds to a cis-acting DNA element (call it D); (2) R and D function as a repressor-operator pair; (3) R functions as a negative regulator of transcription; (4) D is composed of an inverted-repeat sequence; (5) repression by R is dependent on D being supercoiled (Wilson&Tan, 2002).
(a) Based on this information, devise a model to explain the heat-dependent regulation of metabolism in Chlamydia trachomatis.
(b) Some bacteria, like E. coli, use a heat-shock sigma factor to regulate heat-shock transcription. Are the above findings in Chlamydia compatible with use of a heat-sensitive sigma factor?
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