Fluidity is an inherent property of biological membranes and its maintenance (homeoviscous adaptation) is important for optimal functioning of membrane-associated processes. The fluidity of bacterial cytoplasmic membrane increases with temperature or an increase in the proportion of unsaturated fatty acids and vice versa. We found strains deficient in the synthesis of guanine nucleotide analogues (p)ppGpp and lacking FadR, a transcription factor involved in fatty acid metabolism exhibited growth defect that was rescued by an increase in growth temperature or unsaturated fatty acid content. The strain lacking (p)ppGpp was sensitive to genetic or chemical perturbations that decrease the proportion of unsaturated fatty acids over saturated fatty acids. Microscopy showed the growth defect was associated with cell filamentation and lysis and rescued by combined expression of cell division genes ftsQ, ftsA and ftsZ from plasmid. The results implicate (p)ppGpp in the positive regulation of cell division during loss of membrane fluidity. To our knowledge, this is the first report of a (p)ppGpp mediated regulation needed for adaptation to membrane fluidity loss in bacteria.