Can biochemical properties serve as selective pressure for gene selection during inter-species and endosymbiotic lateral gene transfer?
During the evolution of endosymbiosis, only one orthologous gene, either from the invader or the invaded genome, is preserved. Genetic and environmental factors are usually invoked to explain this gene preference. How biochemical parameters can play a role in the selection of genes that code for enzymes that constitute a metabolic pathway is explored. Simple Michaelis-Menten-like enzymes are considered whose kinetic parameters are randomly generated to construct two parallel homologous pathways to account for the contributions of the invaded and the invader. Steady-state fluxes as targets of natural selection are focused. Enzymes are eliminated one by one so that the total flux through the pathway is least disturbed. Analysis of the results, done by different criteria, indicate that the maximal velocities, both forward and backward, are more influential in selection than the respective Michaelis constants. This inclination disappears as metabolite concentrations are increased. It is shown that kinetic selection criteria can result in a mosaicism of enzymes in the same pathway in terms of their genetic origin. Analysis of the results using the control coefficient paradigm disclosed an expected robust correlation between flux control coefficients of enzymes and their selective elimination. Similar analyses, performed for the case of single gene transfer or for gene replication with subsequent mutation, yielded essentially similar results. The results conform with the phenomenon of genetic mosaicism found in phylogenetic analyses of single or double endosymbioses and lateral gene transfer.
Ringemann
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C
Department of Theoretical Biophysics, Institute of Biology, Humboldt University, Invalidenstrasse 42, Berlin 10119, Germany.
Ebenhöh
O
O
Heinrich
R
R
Ginsburg
H
H
D000818:Animals; D003198:Computer Simulation; D019143:Evolution, Molecular; D022761:Gene Transfer, Horizontal / Q000235:genetics*; D006801:Humans; D008957:Models, Genetic; D009097:Multienzyme Complexes / Q000235:genetics*; D010802:Phylogeny; D012641:Selection, Genetic; D015398:Signal Transduction / Q000235:genetics*; D013045:Species Specificity; D013559:Symbiosis / Q000235:genetics*
D009097:Multienzyme Complexes