Dear Colleagues,

The term “antibiotic resistance” implies a phenotype (being resistant to antibiotics) and such phenotype is usually attributed to a “resistance mechanism” (as a mutation in the target of the antibiotic, or the synthesis of an enzyme deactivating the drug, or a pumping out mechanism). However the relation of mechanisms and phenotypes is not necessarily predictable. In fact, the phenotype expected to result from the mechanism might simply not be expressed (at least at the level expected), by a variety of reasons, including gene silencing, recessive condition of the mechanism, insufficient gene copy number, high fitness cost of the expression, inappropriate environmental conditions (studied in ecological genetics), or antagonistic pleiotropy with other resistance gene; also, competition between resistance mechanisms cannot be discarded. Most importantly, the phenotypic expression of a given genetic mechanism might be contingent upon the species (the clones?) where it is located, the growth rate and density of the bacterial population, and, within a particular organism (cell), the expression might be deeply influenced not only by epigenetic interactions, but also by the metabolic status of the cell. In fact the existence of a “mechanism” is the condition for resistance, but there are “processes” required to gain the resistance phenotype. Natural selection of antibiotic resistance is acting on phenotypes, but the ability of selecting the mechanism of resistance, and the carrier organism, is not proportional to the expression of the phenotype; weak (apparently suboptimal) phenotypes could be extremely effective in natural selective conditions. Moreover, the same “mechanism” often provide different phenotypes, not only in terms of level of antibiotic resistance, but on the quality of this resistance (resistance to killing versus resistance to growth inhibition) depending on the antibiotic concentration, the type and physiological features of the target bacterial cell. Indeed the analysis of complex landscape requires of advanced informatic technologies as neural network approach for predicting phenotypes from genotypes The growing dominance of genocentric technology, tending to make synonymous “mechanisms” and “phenotypes” should be modulated by rediscussing the above mentioned asymmetries, and probably others that we do not mention in this summary. This Issue is intending to clarify some of these issues, of critical importance in predicting appropriate antibiotic use and controlling the evolutionary paths and trajectories of antibiotic resistance.

Dr. Fernando Baquero
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Biology is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2200 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

• antibiotic resistance
• resistance phenotypes
• resistance mechanisms
• resistance and metabolism
• phenotype selection
• phenotype–genotype
• phenotype expression
• epigenetics