Gonzalez de Valdivia Ernesto I, Isaksson Leif A
Department of Genetics, Microbiology and Toxicology, Stockholm University, Sweden.
FEBS J. 2005 Oct;272(20):5306-16. doi: 10.1111/j.1742-4658.2005.04926.x.
In Escherichia coli the codons CGG, AGG, UGG or GGG (NGG codons) but not GGN or GNG (where N is non-G) are associated with low expression of a reporter gene, if located at positions +2 to +5. Induction of a lacZ reporter gene with any one of the NGG codons at position +2 to +5 does not influence growth of a normal strain, but growth of a strain with a defective peptidyl-tRNA hydrolase (Pth) enzyme is inhibited. The same codons, if placed at position +7, did not give this effect. Other codons, such as CGU and AGA, at location +2 to +5, did not give any growth inhibition of either the wild-type or the mutant strain. The inhibitory effect on the pth mutant strain by NGG codons at location +5 was suppressed by overexpression of the Pth enzyme from a plasmid. However, the overexpression of cognate tRNAs for AGG or GGG did not rescue from the growth inhibition associated with these codons early in the induced model gene. The data suggest that the NGG codons trigger peptidyl-tRNA drop-off if located at early coding positions in mRNA, thereby strongly reducing gene expression. This does not happen if these codons are located further down in the mRNA at position +7, or later.
在大肠杆菌中，如果密码子CGG、AGG、UGG或GGG（NGG密码子）而非GGN或GNG（其中N为非G）位于+2至+5位置，则与报告基因的低表达相关。在+2至+5位置用任何一种NGG密码子诱导lacZ报告基因，不会影响正常菌株的生长，但会抑制肽基-tRNA水解酶（Pth）有缺陷的菌株的生长。如果将相同的密码子置于+7位置，则不会产生这种效应。其他密码子，如CGU和AGA，位于+2至+5位置时，对野生型或突变型菌株均未产生任何生长抑制作用。通过从质粒中过表达Pth酶，可抑制位于+5位置的NGG密码子对pth突变菌株的抑制作用。然而，过表达与AGG或GGG同源的tRNA并不能挽救诱导模型基因早期与这些密码子相关的生长抑制。数据表明，如果NGG密码子位于mRNA的早期编码位置，会引发肽基-tRNA脱落，从而强烈降低基因表达。如果这些密码子位于mRNA中更靠后的+7位置或更晚位置，则不会发生这种情况。
