Phenotypic profiling of ABC transporter coding genes in Myxococcus xanthus

• Main Authors: Jinyuan eYan, Michael D Bradley, Jannice eFriedman, Roy D Welch
• Format: Article
• Language: English
• Published: Frontiers Media S.A. 2014-07-01
• Series: Frontiers in Microbiology
• Subjects: Myxococcus xanthus; evolution; Biofilm; fitness; multicellularity; phenome
• Online Access: http://journal.frontiersin.org/Journal/10.3389/fmicb.2014.00352/full

Information about a gene sometimes can be deduced by examining the impact of its mutation on phenotype. However, the genome-scale utility of the method is limited because, for nearly all model organisms, the majority of mutations result in little or no observable phenotypic impact. The cause of this is often attributed to robustness or redundancy within the genome, but that is only one plausible hypothesis. We examined a standard set of phenotypic traits, and applied statistical methods commonly used in the study of natural variants to an engineered mutant strain collection representing disruptions in 180 of the 192 ABC transporters within the bacterium Myxococcus xanthus. These strains display continuous variation in their phenotypic distributions, with a small number of outlier strains at both phenotypic extremes, and the majority within a confidence interval about the mean that always includes wild type. Correlation analysis reveals substantial pleiotropy, indicating that the traits do not represent independent variables. The traits measured in this study co-cluster with expression profiles, thereby demonstrating that these changes in phenotype correspond to changes at the molecular level, and therefore can be indirectly connected to changes in the genome. However, the continuous distributions, the pleiotropy, and the placement of wild type always within the confidence interval all indicate that this standard set of M. xanthus phenotypic assays is measuring a narrow range of partially overlapping traits that do not directly reflect fitness. This is likely a significant cause of the observed small phenotypic impact from mutation, and is unrelated to robustness and redundancy.