A 'stemness checkpoint' helps control stem cell identity
Why it matters: This discovery could lead to better laboratory conditions for maintaining stem cells, crucial for drug testing and cell therapies.
- Qi-Long Ying and Austin Smith's 2008 Nature paper established the concept that stem cell self-renewal relies on blocking differentiation signals.
- Researchers from the labs of Qi-Long Ying (USC) and Guang Hu (NIEHS) identified the protein GSK3α as a "stemness checkpoint" that drives differentiation and can be inhibited to maintain stem cell identity.
- GSK3α was shown to be a common checkpoint across diverse stem cell types, including mouse embryonic stem cells (mESCs), epiblast stem cells (mEpiSCs), neural stem cells, and formative stem cells, as well as across species like rats, rabbits, cows, and humans.
- Inhibiting GSK3α allowed mESCs and mEpiSCs to multiply, maintain stable self-renewal, and preserve their identities even when grown together for over a month, demonstrating a shared mechanism for stem cell maintenance.
A new study identifies GSK3α as a universal "stemness checkpoint" that controls the identity of various stem cell types across developmental stages and species, challenging the previous understanding of stem cell maintenance as a sum of unrelated signaling conditions. Researchers from USC and NIEHS found that inhibiting GSK3α allows different stem cells, including mouse embryonic and epiblast stem cells, to maintain their self-renewal and identity even under shared conditions.
