scholarly journals Global metabolic network reorganization by adaptive mutations allows fast growth of Escherichia coli on glycerol

2014 ◽  
Vol 5 (1) ◽  
Author(s):  
Kian-Kai Cheng ◽  
Baek-Seok Lee ◽  
Takeshi Masuda ◽  
Takuro Ito ◽  
Kazutaka Ikeda ◽  
...  
PLoS ONE ◽  
2018 ◽  
Vol 13 (8) ◽  
pp. e0202565 ◽  
Author(s):  
Ignace L. M. M. Tack ◽  
Philippe Nimmegeers ◽  
Simen Akkermans ◽  
Filip Logist ◽  
Jan F. M. Van Impe

1997 ◽  
Vol 41 (9) ◽  
pp. 2059-2060 ◽  
Author(s):  
C Riesenfeld ◽  
M Everett ◽  
L J Piddock ◽  
B G Hall

Mutation to ciprofloxacin resistance continually occurred in nondividing Escherichia coli cells during a 7-day exposure to ciprofloxacin in agar, while no accumulation of rifampin resistance mutations was detected in those cells. We propose that the resistance mutations result from adaptive mutations, which preferentially produce phenotypes that promote growth in nondividing cells.


2020 ◽  
Vol 117 (31) ◽  
pp. 18582-18590 ◽  
Author(s):  
Sandeep Venkataram ◽  
Ross Monasky ◽  
Shohreh H. Sikaroodi ◽  
Sergey Kryazhimskiy ◽  
Betul Kacar

Cells consist of molecular modules which perform vital biological functions. Cellular modules are key units of adaptive evolution because organismal fitness depends on their performance. Theory shows that in rapidly evolving populations, such as those of many microbes, adaptation is driven primarily by common beneficial mutations with large effects, while other mutations behave as if they are effectively neutral. As a consequence, if a module can be improved only by rare and/or weak beneficial mutations, its adaptive evolution would stall. However, such evolutionary stalling has not been empirically demonstrated, and it is unclear to what extent stalling may limit the power of natural selection to improve modules. Here we empirically characterize how natural selection improves the translation machinery (TM), an essential cellular module. We experimentally evolved populations ofEscherichia coliwith genetically perturbed TMs for 1,000 generations. Populations with severe TM defects initially adapted via mutations in the TM, but TM adaptation stalled within about 300 generations. We estimate that the genetic load in our populations incurred by residual TM defects ranges from 0.5 to 19%. Finally, we found evidence that both epistasis and the depletion of the pool of beneficial mutations contributed to evolutionary stalling. Our results suggest that cellular modules may not be fully optimized by natural selection despite the availability of adaptive mutations.


PLoS Genetics ◽  
2017 ◽  
Vol 13 (3) ◽  
pp. e1006702 ◽  
Author(s):  
Elisa Galli ◽  
Caroline Midonet ◽  
Evelyne Paly ◽  
François-Xavier Barre

2013 ◽  
Vol 38 (27) ◽  
pp. 11780-11789 ◽  
Author(s):  
Jenni J. Seppälä ◽  
Antti Larjo ◽  
Tommi Aho ◽  
Olli Yli-Harja ◽  
Matti T. Karp ◽  
...  

2002 ◽  
Vol 184 (20) ◽  
pp. 5599-5608 ◽  
Author(s):  
Cesar Rodriguez ◽  
Joshua Tompkin ◽  
Jill Hazel ◽  
Patricia L. Foster

ABSTRACT Adaptive mutation to Lac+ in Escherichia coli strain FC40 depends on recombination functions and is enhanced by the expression of conjugal functions. To test the hypothesis that the conjugal function that is important for adaptive mutation is the production of a single-strand nick at the conjugal origin, we supplied an exogenous nicking enzyme, the gene II protein (gIIp) of bacteriophage f1, and placed its target sequence near the lac allele. When both gIIp and its target site were present, adaptive mutation was stimulated three- to fourfold. Like normal adaptive mutations, gIIp-induced mutations were recA+ and ruvC+ dependent and were mainly single-base deletions in runs of iterated bases. In addition, gIIp with its target site could substitute for conjugal functions in adaptive mutation. These results support the hypothesis that nicking at the conjugal origin initiates the recombination that produces adaptive mutations in this strain of E. coli, and they suggest that nicking may be the only conjugal function required for adaptive mutation.


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