The human gut microbiota is required for the degradation of otherwise undigestible dietary and host-derived polysaccharides. These polysaccharides are a key energy source for the gut microbiota and fermentation products such as short chain fatty acids are beneficial to the human host. The Bacteroidetes are the prominent contributors to polysaccharide degradation in the gut and the model system for this degradation is the starch utilization system (Sus) in Bacteroides thetaiotaomicron (Bt). All Sus-like systems contain three key components: 1. a SusC-like protein, a hypothesized TonB-dependent transporter; 2. a SusD-like protein, an accessory polysaccharide-binding protein; and 3. a transcriptional regulator, SusR in the Sus system. Despite the importance of the SusC-like protein in these systems, little work has been done to confirm the TonB-dependence of transport through these proteins or to characterize the TonB-SusC pair. To address this question, we have generated Bt strains in which each of the 12 TonB genes are deleted. Using these single mutant strains, we have shown that under normal lab growth conditions, one TonB is important but not essential for proper function of SusC and growth on starch. Using membrane proteomics, we have shown changes in the abundance of other TonB proteins when this important TonB is deleted suggesting redundancy in function of these TonB proteins. This mechanistic understanding of how Bt and related Bacteroidetes use polysaccharides to establish their niche in the microbiota will allow us to design non-invasive approaches for optimizing the gut community and improving patient outcomes caused by a lack or overgrowth of Bacteroidetes.