Mutant bacteria

The ansa-chain of the ansamycins streptovaricins (4), rifamycins (263), geldanamycin (4), and herbimycin (32) has been shown to be polyketide in origin, being made up of propionate and acetate units with the 0-methyl groups coming from methionine. The remaining aromatic C N portion of the ansamacroHdes is derived from 3-amino-5-hydroxybenzoic acid (264—266) which is formed via shikimate precursors. Based on the precursors of the rifamycins and streptovaricins isolated from mutant bacteria strains, a detailed scheme for the biosynthesis of most of the ansamacroHdes has been proposed (95,263). 

In 1991, several factors were demonstrated to affect the efficiency of relE controlled killing of E. colt when under lac promoter control (Knudsen Karlstrom, 1991)- Cells escaped suicide primarily because of the mutation rate and the leakiness of repression during normal growth. When relF was under lac JV5 promoter/operator control, the inactivation of suicide function through spontaneous mutation occurred at a frequency of <5 x 10 9. Knudsen has further theorized that if the number of suicide minus (mutant) bacteria in a culture can be kept at zero before induction, all cells will die. This can be achieved in two ways provide the suicide function in duplicate, and control the suicide gene expression so stringently, with a chromosomally located laclq gene, that a basal level of the suicide function to which cells can adapt will not be present (Knudsen et al., 1995). 

The essential stages of the multistep route used by nature to synthesize aromatic amino acids were elucidated in the 1950s by studies on mutant bacteria (e.g. Aerobacter and Escheridiia coi) the cyclization of D-glucose (17) to 5-dehy-droquinic acid (18) and the formation of shikimic acid (19) [28], The first aromatic compound in the reaction chain is anthranilic acid (20) ... 

The use of genetic mutants determined the complex pathways that lead to the amino acids. A mutant is an organism that has a different DNA sequence from its parent(s). Mutant bacteria that require a specific compound for growth are called auxotrophs. The first step in pathway determination is to assemble a large collection of auxotrophic mutants that can t make the compound of interest. 

If the two DNAs have the same sequence, they can form a Holliday junction, but no detectable genetic recombination takes place because no information change has occurred. If the two DNAs are very different, no recombination will take place because formation of a Holliday junction requires homologous information. If the two DNAs of the Holliday junction are similar to each other but not identical (that is, they contain mismatches), then repair enzymes, which remove the base and/or nucleotide from one of the mismatched strands, will repair the DNA. The fact that some enzymes participate both in repair and in recombination accounts for the fact that many recombination-deficient mutant bacteria are also highly sensitive to ultraviolet light. 

Zhao X, Drlica K. Restricting the selection of antibiotic-resistant mutant bacteria measurement and potential use of the mutant selection window./. Infect. Dis., 2002, 185, 561-565. 

Everything pointed to the N2-binding site being a metal atom in the MoFe-protein, probably Mo itself, but it remained elusive. Evidence that the site had to be sterically close to the Mo atom was in due course obtained using mutant bacteria (see Section 5, below). 

The resistant mutant bacteria do not transport or accumulate tetracycline. This plasmid-controlled resistance is transmitted by transduction or by conjugation. 

According to Nissen et al. [27], proteins L4, L22, and L39e (the letter e represents a protein in a bacterial SOS ribosomal subunit, a protein that belongs to one of the homologs in eukaryotic 60S ribosomal subunit) have been shown to be present in the polypeptide exit tunnel [average diameter, about IS A length of the tunnel, 100 A (Fig. 3B)] present in the SOS ribosomal subunit from H. maris-mortui. Six other proteins (L19, L22, L23, L24, L29, and L31e) are known to be located in the exit area of the polypeptide tunnel [26, 27]. If these proteins are involved in the inhibitory actions of macrolide antibiotics, mutant bacteria resistant to macrolides will develop in the future. 

Early studies of J. Adler have demonstrated that, in E. coli, the chemoattractants themselves are detected [6, 9] rather than their metabolic products. This conclusion was based on two types of observations. One was that mutant bacteria, which have lost the ability of metabolizing or transporting a chemical, can nevertheless be attracted to the chemical. The other type of observation was that nonmetabolizable analogs of metabolizable chemicals (e.g., D-fucose, a-methyl-DL-aspartate, or a-aminoisobutyrate— analogs of D-galactose, L-aspartate, or L-serine, respectively) attract bacteria. In contrast, some metabolizable chemicals... 

However, this solution could not be appreciated by normal consumers because of the hypothetical microbial dissemination - by breakage - in the environment. Naturally, the consumer should be informed about the absence of real risks associated to Lactobacillaceae or moulds, but the acceptance of a similar device is not sure. Existing regulations are not ready to accept the authorised release of living indicators. In addition, there are two risks to be considered (1) the eventuality of mutant bacteria and (2) the release of powerful bacteriophages. For these reasons, living indicators may be proposed as monitoring instruments for manufacturers and official inspectors only. 

Amber mutants mutant bacteria in which the mRNA contains the codon UAG as a result of a point mutation (see Amber codon). The mutation is not necessarily lethal, because a compensatory suppressor mutation in a tRNA may enable the protein synthesizing system to recognize the amber codon as a sense codon. The term amber was arbitrarily chosen by the discoverer of A. m. 

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