Required to repress ESX-1-mediated secretion under low ATP conditions. This function requires the ATP-binding motif. Residues 1-81 interact with EsxB while residues 35-186 interact with an artificial EsxB-EsxA heterodimer (PubMed:19854905). Double espI-eccD1 mutants abolish EsxA and EsxB secretion, but not their expression (PubMed:14557547). One group has shown no growth in the human macrophage-like cell line THP-1, no cytotoxicity, attenutated infection in mice, nearly 100-fold less bacteria in lung and spleen of C57BL/6; Brodin et al., attribute this result to polar effects on the downstream gene (PubMed:14756778, PubMed:16368961). Another group has shown that inactivation does not abolish EsxA (ESAT-6) secretion, EsxA-specific immunogenicity or virulence (PubMed:16368961, PubMed:25039394).