Molecular Biology and Evolution, Vol 13, 719-734, Copyright © 1996 by Society for Molecular Biology and Evolution
M Taylor and R Feyereisen
To the prevailing biochemical/physiological classification of mechanisms of
organismal resistance to toxicants, an additional molecular dimension is
proposed. Predictions are developed regarding the relative prevalence of
different classes of mutations and are found to compare favorably with
reports from the literature. In particular, point mutations in target loci
were the dominant form of resistance for both lab and field selection.
Amplifications of target loci were less common than structural mutations,
and more common for lab-selected than for field-selected strains.
Amplification was the most common mechanism of up-regulation of
metabolizing enzymes. In comparison, only one mutation involving
cis-regulation and several involving trans-acting regulation were found.
Mutations involving gene disruption and down- regulation were uncommon, but
were found in appropriate cases, i.e., when toxicants stimulated rather
than inhibited target function and when metabolizing enzymes converted
toxicants into more toxic metabolites. Additional phenomena of likely but
uncertain importance are genetic "succession," recombinational limitation,
and negative cross-resistance. More work on these phenomena and on
quantification of fitness costs of resistance is recommended.
REVIEW ARTICLE
Molecular biology and evolution of resistance of toxicants
Department of Entomology, University of Arizona.
![]()
CiteULike
Connotea
Del.icio.us What's this?
This article has been cited by other articles:
![]() |
T. G. Wilson Drosophila: Sentinels of Environmental Toxicants Integr. Comp. Biol., January 1, 2005; 45(1): 127 - 136. [Abstract] [Full Text] [PDF] |
||||
![]() |
S. M. Bello, D. G. Franks, J. J. Stegeman, and M. E. Hahn Acquired Resistance to Ah Receptor Agonists in a Population of Atlantic Killifish (Fundulus heteroclitus) Inhabiting a Marine Superfund Site: In Vivo and in Vitro Studies on the Inducibility of Xenobiotic Metabolizing Enzymes Toxicol. Sci., March 1, 2001; 60(1): 77 - 91. [Abstract] [Full Text] [PDF] |
||||
![]() |
L. E. Cowen, D. Sanglard, D. Calabrese, C. Sirjusingh, J. B. Anderson, and L. M. Kohn Evolution of Drug Resistance in Experimental Populations of Candida albicans J. Bacteriol., March 15, 2000; 182(6): 1515 - 1522. [Abstract] [Full Text] |
||||
![]() |
L. E. Cowen, C. Sirjusingh, R. C. Summerbell, S. Walmsley, S. Richardson, L. M. Kohn, and J. B. Anderson Multilocus Genotypes and DNA Fingerprints Do Not Predict Variation in Azole Resistance among Clinical Isolates of Candida albicans Antimicrob. Agents Chemother., December 1, 1999; 43(12): 2930 - 2938. [Abstract] [Full Text] |
||||
![]() |
J. D. Evans and D. E. Wheeler Differential gene expression between developing queens and workers in the honey bee, Apis mellifera PNAS, May 11, 1999; 96(10): 5575 - 5580. [Abstract] [Full Text] [PDF] |
||||
![]() |
D. Lee, Y. Park, T. M. Brown, and M. E. Adams Altered Properties of Neuronal Sodium Channels Associated with Genetic Resistance to Pyrethroids Mol. Pharmacol., March 1, 1999; 55(3): 584 - 593. [Abstract] [Full Text] |
||||
![]() |
R. Feyereisen Juvenile hormone resistance: ¡ no PASaran ! PNAS, March 17, 1998; 95(6): 2725 - 2726. [Full Text] [PDF] |
||||





