Although the nature of DNA sequences causing transcription arrest is not known, the mechanism of transcription arrest and the roles of GreA and GreB in restoring elongation can be explained in the framework of 'inchworm model' described above. The transcription arrest may result when the catalytic site of RNAP is misplaced from the 3' end of growing transcript. This, itself may result, if the 'lagging product site' slipped backward on the template, bringing the catalytic site out of register. Transcript cleavage by GreB would create a new 3' end into the right register, thus restoring elongation. Further, at some template sites, translocation may disturb the placement of catalytic site into the right register, and GreA-induced cleavage of short segments might restore the appropriate register to resume elongation. Thus an elongation barrier may be overcome by RNAP through a 'backup and restart' mechanism.
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