Streptococcus agalactiae, or GBS; is a commensal bacterium of the gastrointestinal and urogenital tract. First identified in cattle, it rapidly became the major cause of neonatal infections in humans, due to mother-to-fetus transmission during delivery. In order to persist in a variety of environments, S. agalactiae requires nutrients. Among these, we are particularly interested in zinc, an essential microelement for the bacterium, but present in free form only in trace amounts in humans and sometimes «sequestered» by the immune system during infection. We observed that S. agalactiae was particularly resistant to zinc deficiency. Using RNA seq approach, we identified genes overexpressed in zinc-deficient conditions, and therefore potentially involved in resistance to this deficiency. We were thus able to characterize the first zinc transporter in S. agalactiae: the Adc/Lmb transporter, made up of 7 different proteins and capable of binding zinc with a very high affinity. Its role in vivo in the virulence of the bacterium has been demonstrated. The rpsN gene, which encodes a subunit of the ribosomal protein S14, is also one of the most strongly regulated genes. We demonstrated that rpsN expression is dependant on AdcR, a regulatory protein involved in zinc homeostasis in S. agalactiae. The regulation of rpsN by AdcR is unusual in that we have shown that the regulator binds to the promoter region of rpsN through 3 “AdcR boxes” whose relative importance has been determined. We are also interested in the function of the RpsN protein, which appears to be involved in a “protein switch” phenomenon with its paralog, RpsNa, which requires zinc to function. The impact of RpsN deletion on the ability of S. agalactiae to resist zinc deficiency and its importance with respect to the Adc/lmb transporter was studied.