Extended Data Fig. 9: Model for how AIRIM and AFG2B variants cause differentiation defects in human cerebral organoids. | Nature Cell Biology

Extended Data Fig. 9: Model for how AIRIM and AFG2B variants cause differentiation defects in human cerebral organoids.

From: A programmed decline in ribosome levels governs human early neurodevelopment

Extended Data Fig. 9

(Top) The 55LCC complex promotes the maturation of the pre-60S subunit by fostering RSL24D1 recycling. Normal levels of mature 60S subunits allow for the normal differentiation of cerebral organoids. (Bottom) Allelic variants in AIRIM and AFG2B perturb the function of the 55LCC complex, compromising the maturation of pre-60S subunits. This results in reduced protein synthesis capacity in cerebral organoids, marked by delayed differentiation, reduced size, increased apoptosis, and mitochondrial defects.

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