Inability to catabolize galactose leads to increased ability to compete for nodule occupancy in Sinorhizobium meliloti

Abstract

A mutant unable to utilize galactose was isolated in Sinorhizobium meliloti strain Rm1021. The mutation was found to be in a gene annotated dgoK1, a putative 2-keto-3-deoxygalactonokinase. The genetic region was isolated on a complementingcosmid and subsequently characterized. Based on genetic and bioinformatic evidence, the locus encodes all five enzymes (galD, dgoK, dgoA, SMc00883, and ilvD1) involved in the De Ley-Doudoroff pathway for galactose catabolism. Although all five genes are present, genetic analysis suggests that the galactonase (SMc00883) and the dehydratase (ilvD1) are dispensable with respect to the ability to catabolize galactose. In addition, we show that the transport of galactose is partially facilitated by the arabinose transporter (AraABC) and that both glucose and galactose compete with arabinose for transport. Quantitative reverse transcription-PCR (qRT-PCR) data show that in a dgoK background, the galactose locus is constitutivelyexpressed, and the induction of the ara locus seems to be enhanced. Assays of competition for nodule occupancy show that the inability to catabolize galactose is correlated with an increased ability to compete for nodule occupancy. © 2012, American Society for Microbiology.