Juan Jauregui-Lozano: How Replication Stress Impairs Red Blood Cell Maturation
Juan Jauregui-Lozano, Postdoctoral Fellow at Department of Biomedicine, shared a post on LinkedIn:
“So excited to finally see this preprinted!
What began as a ‘side-quest’ to find tools that raise R-loop levels became a full project on understanding how replication stress impairs red blood cell production.
We found that at sub-lethal doses, mechanistically distinct genotoxic drugs converge on a strikingly similar effect: erythroid progenitors differentiate prematurely but fail to enucleate and mature. Inhibiting ATR, but not ATM, phenocopied the genotoxic insults.
This convergence suggests homeostasis of the replication stress ATR axis plays an important role in regulating erythroid output. We then performed scRNA-seq of CD34+ HSPCs undergoing erythropoiesis to map drug effects across erythroid differentiation at single-cell resolution, and found just how (very!) similar the drugs’ transcriptomic effects were.
We also found that replication stress pushes a fraction of late erythroblasts into an aberrant, p21/p53-high state with an immature hemoblogin or erythroid profile. Together, our findings point to an additional mechanism that could contribute to chemotherapy-associated anemia, though this remains to be tested in vivo.
This has been a really fun project that allowed me to go back to my PhD roots, combining experimental and computational biology to piece together the bigger picture. Thanks to co-authors Amandine Kremer and Karin Prummel, and to my PI Judith Zaugg.
Thanks also to Department of Biomedicine, Human Frontier Science Program (HFSP) and the University of Basel Vice-president’s Office of Research for their generous support. And a genuine thank you to the moms who donated cord blood. This work couldn’t exist without you all!”
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