Paralogous guanine deaminases acquired from bacteria by horizontal gene transfer promote purine homeostasis in Caenorhabditis elegans.

Caenorhabditis elegans xdh-1 deficiency leads to rare xanthine stone formation, and loss of gda-1 intestinal guanine deaminase exacerbates this phenotype.

• Why it matters: Purine metabolism disruptions underlie disorders such as xanthinuria, but the genetic and spatial regulators of purine homeostasis in animals remain unclear.
• What they did: The authors built an xdh-1 deficiency model and ran a forward genetic screen for mutations that increase xanthine stones, identifying gda-1 as an intestinal guanine deaminase; they also analyzed the paralog gda-2 and its bacterial origin.
• The result: gda-2 shares guanine deaminase activity and can compensate for gda-1 in guanine metabolism, yet gda-1 and gda-2 have non-redundant roles in xanthine accumulation and stone formation, implying horizontally acquired bacterial genes shaped nematode purine catabolism.

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