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Agonists of the adenylyl cyclase Rv1625c are a novel drug class that selectively inhibits Mtb growth in macrophages and cholesterol-rich conditions by an unknown mechanism. Combining condition-resolved transcriptomics, genome-scale metabolic modeling, and genetic perturbation, we show these agonists cause a blockade in the electron transport chain, which likely activates Rv1625c. The elevated cAMP in turn drives global transcriptional and post-translational remodeling of central carbon and lipid metabolism. The resulting methylcitrate cycle reversal chokes cholesterol breakdown products from entering central metabolism, diverting carbon toward cell wall and virulence-lipid (phthiocerol dimycocerosate) synthesis and inhibiting growth. These drugs thus hijack an endogenous switch that reroutes carbon from biomass to virulence-lipid production. Hence, nutrients that restore carbon flux and relieve ETC blockade reduce activity, whereas Rv1625c overexpression and ETC inhibitors potentiate drug action even in refractory conditions.\n                <\/jats:p>","DOI":"10.64898\/2026.09.10.750769","type":"posted-content","created":{"date-parts":[[2026,9,17]],"date-time":"2026-09-17T04:38:00Z","timestamp":1789619880000},"source":"Crossref","is-referenced-by-count":0,"title":["An adenylyl cyclase switch reroutes carbon from growth to virulence lipids in\n                  <i>Mycobacterium tuberculosis<\/i>"],"prefix":"10.64898","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-3642-9605","authenticated-orcid":false,"given":"Selva Rupa Christinal","family":"Immanuel","sequence":"first","affiliation":[{"name":"Institute for Systems Biology, Seattle, WA 98109, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Julie","family":"Do","sequence":"additional","affiliation":[{"name":"Institute for Systems Biology, Seattle, WA 98109, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-2934-5267","authenticated-orcid":false,"given":"Eliza J. 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