This family consists of the Gns/GnsA/GnsB proteins. GnsA and GnsB are multicopy suppressors of the cold-sensitive secG null mutation. These proteins participate in the synthesis of phospholipids, suggesting the functional relationship between SecG and membrane phospholipids. Overexpression of gnsA and gnsB causes a remarkable increase in the unsaturated fatty acid content. However, the gnsA-gnsB double null mutant exhibits no effect. Both proteins are predicted to possess a helix-turn-helix structure [].
