| - | In E. coli, the SecM nascent polypeptide causes elongation arrest, while, interacting with 23S RNA bases A2058 and A749-753 in the exit tunnel of, the large ribosomal subunit. We compared atomic models fitted by, real-space refinement into cryo-electron microscopy reconstructions of a, pretranslocational and SecM-stalled E. coli ribosome complex. A cascade of, RNA rearrangements propagates from the exit tunnel throughout the large, subunit, affecting intersubunit bridges and tRNA positions, which in turn, reorient small subunit RNA elements. Elongation arrest could result from, the inhibition of mRNA.(tRNAs) translocation, E site tRNA egress, and, perhaps translation factor activation at the GTPase-associated center. Our, study suggests that the specific secondary and tertiary arrangement of, ribosomal RNA provides the basis for internal signal transduction within, the ribosome. Thus, the ribosome may itself have the ability to regulate, its progression through translation by modulating its structure and, consequently its receptivity to activation by cofactors.
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| - | Elongation arrest by SecM via a cascade of ribosomal RNA rearrangements., Mitra K, Schaffitzel C, Fabiola F, Chapman MS, Ban N, Frank J, Mol Cell. 2006 May 19;22(4):533-43. PMID:[http://ispc.weizmann.ac.il//pmbin/getpm?pmid=16713583 16713583]
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