September 28, 2025Open Access

RPS19 and RPL5 Haploinsufficient Models Reveal Divergent Ribosomal Subunit Controls of Fetal Hematopoiesis

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Novel in vivo models reveal how RPL5 and RPS19 haploinsufficiencies impact fetal hematopoiesis, suggesting different cellular mechanisms involved.

RPL5 and RPS19 haploinsufficiencies exhibit divergent roles in fetal hematopoiesis.
RPL5 impairment causes HSPC accumulation and prenatal lethality via p53-mediated ferroptosis.
RPS19 deficiency depletes HSPCs and impairs erythroid expansion through p53-dependent apoptosis.
Deletion of Runx1 in RPS19-haploinsufficient mice partially rescues HSPC numbers.

Blanc et al. (2025) studied this question.

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Novel in vivo models reveal how RPL5 and RPS19 haploinsufficiencies impact fetal hematopoiesis, suggesting different cellular mechanisms involved.