S-adenosyl-L-homocysteine triggers an adaptive response that extends lifespan through the YBT1 ABC transporter.

SAH triggers an adaptive response that extends yeast lifespan by activating Ybt1, an ABC transporter, through a hormetic mechanism involving ROS production.

• Why it matters: Understanding how metabolic signals influence aging can reveal targets for lifespan extension; the role of SAH as a signaling molecule remains unclear.
• What they did: The study used yeast models to show that transient ROS production induced by SAH during early growth mimics partial SAH hydrolase inhibition, extending CLS, with Ybt1 identified as a key downstream effector.
• The result: Overexpression of YBT1 extends CLS by engaging pathways such as TORC1 downregulation, autophagy, and AMPK activation, suggesting SAH acts as a metabolic signal linking nutrient status to longevity.