Previous work showed that Group A Streptococcus (GAS) modulates host cell metabolism to induce production and extracellular release of asparagine (ASN). ASN is sensed by GAS and alters the transcription of 17% of its genes including the quorum sensing (QS) locus, sil. As other Gram-positive QS loci, sil senses the autoinducer peptide, SilCR, via the two-component system (TCS) SilA/B. This induces SilCR own production, a process known as autoinduction. In strain JS12 aoutoinduction leads to bacteriocin production that kill other GAS strains. In the current work, we demonstrate that sensing of ASN by GAS upregulates the expression of SilCR independently of SilA/B. This consequently switches on the autoinduction cycle of SilCR production. The autoinduction process propagates throughout the GAS population, resulting in synchronous production of bacteriocins.