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Abstract
The primary objective of this work was to further characterize two transcriptional regulators that were previously identified in our lab. One regulator, Agl3R, belongs to the GntR family of transcriptional regulators. During this study I showed that Agl3R was a repressor of its own transcription as well as that of the adjacent ATP-binding cassette transporter, encoded by agl3ABC. A transposon insertion mutant of the agl3R open reading frame exhibited a whiphenotype and failed to produce the antibiotic actinorhodin. Deletion of the agl3ABC cluster restored the wild-type phenotype to an agl3Rmutant leading to the suggestion that overexpression of the ABC transporter was responsible for the phenotype, and that excessiveexpression of agl3ABCmay allow for improper importation of a developmental signal. The second regulator, XdhR, is a member of the TetR family of transcriptional regulators and is located directly adjacent to a molybdopterin binding cluster, xdhABC, encoding an enzyme with xanthine dehydrogenase (XDH) activity. A deletion mutant for the xdhRopen reading frame was bld and overproduced the blue pigment associated with actinorhodin production. Idetermined that XdhR was a transcriptional repressor of its own synthesis as well of that of the adjacent xdhABC cluster. I suggested that over expression of an enzyme with XDH activity might cause a signaling breakdown due to manipulation of the GTP pool and the amount of ppGpp(p) present in the cell.Index Words: Streptomyces, ATP-binding cassette transporter, xanthine dehydrogenase, GntR regulator, TetR regulatorq