Ivan Matic - Selected Publications#
1) Matic, I., Radman, M., Taddei, F., Picard, B., Doit, C., Binguen, E., Denamur, E. and Elion, J. Highly variable mutation rates in commensal and pathogenic Escherichia coli. Science (1997) 277: 1833-1834.
This article shows that, contrary to theoretical predictions, strong mutator strains are not rare in natural bacterial populations. Observed strong mutator phenotypes results from inactivation of genes coding for mismatch repair system that assures accuracy of DNA replications and controls homologous recombination. When adaptation is limited by the available genetic variability, natural selection favors cells having high mutation rates in bacterial populations. High mutation rates can be advantageous because they increase the probability of generation of beneficial mutations.
2) Denamur, E., Lecointre, G., Darlu, P, Tenaillon O, Acquaviva, C., Sayada, S., Sunjevaric, I., Rothstein, R., Elion, J., Taddei, F., Radman, M. and Matic, I. (2000) Evolutionary implications of the frequent horizontal transfer of mismatch repair genes. Cell 103: 711-721
This study reveals important mechanism of the bacterial adaptive evolution, which involves modulation of mutation and recombination rates by recurrent losses and reacquisitions of mismatch repair gene functions.
3) Bjedov, I., Tenaillon, O., Gérard, Souza, V., Denamur, E., Radman, M., Taddei, F., and Matic, I. (2003) Stress-Induced Mutagenesis in Bacteria. Science 300:1404-1409.
The possibility of adapting the mutation rate to environmental conditions is interesting from an evolutionary point of view. Stress-induced mutagenesis allows rapid adaptation to complex environmental challenges without compromising the population fitness because it reduces the overall cost of a high mutation rate. This study shows that stress-inducible mutagenesis is widespread phenomenon in E. coli natural populations. High variability of the stress-inducible mutagenesis reflects the diversity of selective pressures in different environments. This study provides evidence that the evolution of stress-inducible mutation rates is rapid at the evolutionary time scale.
4) Baeriswyl, S., Diard, M., Mosser, T., Leroy, M., Maniere, X., Taddei, F., and Matic, I. (2010) Modulation of aging profiles in genetically identical Caenorhabditis elegans by bacteria causing different extrinsic mortality rates, Biogerontology, 11 : 53 - 65
This study shows that the high extrinsic mortality imposed by the pathogens results in the modulation of nematodes’ life-history traits, including aging and reproduction, which could be an adaptive response aiming at the maximization of Darwinian fitness. Such scenario would fit into the dispensable soma theory, which explains aging as a result of the optimization of resources between maintenance and repair of its soma and the reproductive functions.
5) Diard, M., Garry, L., Selva, M., Mosser, T., Denamur, E., and Matic, I. (2010) Extra-Intestinal Pathogenic Escherichia coli Pathogenicity Associated Islands are Fitness Elements Involved in the Intestinal Colonization. J Bacteriol 192 : 4885-4893
This study shows that virulence of the extraintestinal E. coli pathogenic strains, which frequently cause disease in the host in which they asymptomatically colonize the intestine, is most likely the consequence of commensalism. These results are in accordance with the coincidental-evolution hypothesis postulating the virulence of many human pathogens is not an evolutionarily selected trait, but an accidental by-product of the selection that operates in another ecological context.
6) Gutierrez, A., Laureti, L., Crussard, S., Abida, H., Rodríguez Rojas, A., Blázquez, J., Baharoglu, Z., Mazel, D., Darfeuille, F., Vogel, J., and Matic, I (2013)Beta-lactam antibiotics promote mutagenesis via RpoS-mediated replication fidelity reduction, Nature Communications, 4: 1610, doi:10.1038/ncomms2607
This study reports that subinhibitory concentrations of bactericidal antibiotics induce mutagenesis in several Gram-negative bacterial species. Mutagenesis induced by subinhibitory concentrations of antibiotics requires RpoS-controlled general stress response induction, PolIV error-prone DNA polymerase and the reduction of the of the DNA-replication fidelity control by mismatch-repair. The reduction in mismatch-repair activity is mediated by SdsR, the RpoS-controlled small RNA. Therefore, this study present important demonstration that stress-induced mutagenesis is genetically controlled process and not unavoidable secondary consequence of stress.
7) Elez, M., Murray, A., Bi, L.B., Zhang, X.E., Matic*, I. and Radman* M. (2010) Seeing mutations in living cells. Curr. Biol. 20:1432-1437. (*thèse authors have equaly contributed to this work)
Mutations are very rare and therefore hard to detect, particularly as they emerge. Previously, mutations have been found by detecting altered phenotypes or sequencing complete genomes, but most mutations do not have overt phenotypes and sequencing is expensive and has limited time resolution. In addition, in order to sequence genomes, cells must be killed. This article reports development of a novel mutations assay that allows for the first time monitoring genome-wide spontaneous mutation rates in living cells independently of their effect on fitness: i.e., lethal, deleterious and even neutral mutations can be visualized.
8) Laureti, L., Selva, M., Dairou, J., and Matic, I (2013) Reduction of dNTP levels enhances DNA replication fidelity in vivo. DNA Repair, 13 :300-305
The search of antimutator strains has always been of considerable interest given that they can delve into the real sources and mechanisms of spontaneous mutation rate, when all mutation-prevention systems are operative. This work is the first demonstration that the intracellular energy supply plays an important role in the modulation of spontaneous mutation rate in E. coli.
9) Giroux, X., Su, W-L., Bredeche, M-F., and Matic, I. (2017). Maladaptive DNA repair activity is the ultimate contributor to the death of trimethoprim-treated cells under aerobic and anaerobic conditions. PNAS USA, 114:11512-11517
The bactericidal effects of antibiotics are undoubtedly triggered by target-specific interactions. However, this work shows that antibiotic treatment-induced cell death is ultimately caused by the metabolic perturbations and maladaptive DNA repair that kill cells by fragmenting their genome.
10) Woo, A.C., Faure, L., Dapa, T., and Matic, I. (2018). Heterogeneity of spontaneous DNA replication errors in single isogenic Escherichia coli cells. Sci Adv 4, eaat1608.
Mutations are the primary source of genetic variation, without which there is no evolution. Therefore, understanding how mutations arise is fundamental for the understanding of evolution of the living systems. This article reports that spontaneous mutations in proliferating cells arose more frequently in the subpopulations suffering endogenous stresses, such as problems with proteostasis, genome maintenance and reactive oxidative species production. The presence of such subpopulations of phenotypic mutators is not expected to affect the average mutation frequency and to reduce the population mean fitness in a stable environment. However, they can contribute to the population adaptability in fluctuating environments because they represent a reservoir of increased genetic variability.
