The degree to which surface motile bacteria explore their surroundings is influenced by aspects of their local environment. Accordingly, regulation of surface motility is controlled by numerous chemical, physical, and biological stimuli. Discernment of such regulation due to these multiple cues is a formidable challenge. Additionally inherent ambiguity and variability from the assays used to assess surface motility can be an obstacle to clear delineation of regulated surface motility behavior. Numerous studies have reported single environmental determinants of microbial motility and lifestyle behavior but the translation of these data to understand surface motility and bacterial colonization of human host or environmental surfaces is unclear. Here, we describe the current state of the field and our understanding of exogenous factors that influence bacterial surface motility.

BackgroundHuman requirements for dietary selenium are met mainly by crops. However, excessive uptake of selenium in plants can restrict growth, and its toxicity has been postulated to target roots. Selenite toxicity can be attributed to its assimilation into selenocysteine, which can replace cysteine to yield malformed selenoproteins. Additionally, selenite has pro-oxidant properties. In this study, the effects of selenite on root tissue in Brassica napus (canola) were investigated to better understand its mode of toxicity and the metabolic adjustments needed to mediate a selenite-response.ResultsSelenite induced the rapid formation of mitochondrial superoxide, which led to decreased aconitase activity and involvement of the alternative oxidase pathway. Although selenite altered primary metabolism, as observed by the increased amino acids and decreased TCA cycle metabolites, increased glucose presumably supported higher respiratory rates and ATP levels reported in this study. Additionally, evidence is presented indicating that selenite suppressed the ubiquitin-proteasome pathway, and induced the pentose phosphate pathway needed to maintain antioxidant metabolism. Selenite treatment also elevated glutathione concentration and coincided with increased levels of γ-glutamyl cyclotransferase, which may possibly degrade selenium metabolites conjugated to glutathione.ConclusionCollectively, the data indicate that selenite necessitates the reconfiguration of metabolic pathways to overcome the consequences of mitochondrial oxidative stress in root tissue. Efforts to mitigate the detrimental effects of selenite-induced oxidative stress may ultimately improve selenium tolerance and accumulation in crops.Electronic supplementary materialThe online version of this article (doi:10.1186/s12870-014-0259-6) contains supplementary material, which is available to authorized users.

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