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Perez Acebron, S.

Publications and source records attributed to Perez Acebron, S..

2 recordsLinked to original sources

Long-term prevention of aneuploidy in human pluripotent stem cells by fine-tuning GSK3 activity

Human pluripotent stem cells (hPSCs) are critical cell sources to model human development and hold promise towards regenerative medicine. However, cultured hPSCs quickly acquire chromosome gains or losses (aneuploidy) due to high replicative stress and errors in chromosome segregation, which hampers their use for stem cell therapies. We have recently described that embryo patterning signals control chromosome segregation fidelity during early human lineage specification by modulating the response to replicative stress. Here, we demonstrate that fine-tuned activation of WNT signalling using off-the-shelf GSK3 inhibitors prevents chromosome missegregation and aneuploidy during long term passaging of hPSCs. Lineage-specification and sequencing analyses demonstrate that hPSCs culture with E8 supplemented with a low dosage of GSK3 inhibitors retain primed pluripotency and full potential to the differentiation into the 3 germ layers for over 30 passages. Strikingly, detailed mitotic studies revealed that long-term cultured hPSCs often display ultra-fine chromosome bridges during anaphase due to unreplicated DNA, which can result in hitherto uncharacterised copy-number-variations and other genomic aberrations. We show that culture with low dosage of the GSK3 inhibitor CHIR99021, but not direct attenuation of DNA replication stress using nucleosides, prevents mitotic DNA synthesis and the formation of ultra-fine bridges during long term hPSC passage. Taken together, we propose to enrich E8 culture media with 100 nM CHIR99021 to maintain euploidy in primed hPSCs, and to routinely map for genomic alterations, in addition to aneuploidy, for modelling and regenerative medicine studies.

cell biology↗

Wnt10b signaling regulates replication stress-induced chromosomal instability in human cancer

Wnt signaling pathways are involved in various developmental and tissue maintenance functions while deregulated Wnt signaling is closely linked to human cancer. Recent work revealed that loss of Wnt signaling impairs mitosis and causes abnormal microtubule growth at the mitotic spindle resulting in chromosome missegregation and aneuploidy, both of which are hallmarks of cancer cells exhibiting chromosomal instability (CIN). Here, we demonstrate that Wnt signaling specifically activated by Wnt10b is relevant in colorectal cancer cells to prevent abnormal microtubule dynamics and chromosome missegregation. Although mitosis is affected, Wnt10b signaling is required during the S phase of the cell cycle. In fact, Wnt10b signaling acts upon DNA replication stress in S phase, a condition typically associated with CIN in cancer, to prevent increased microtubule dynamics from S phase until mitosis, where they otherwise manifest in chromosome missegregation. Interestingly, replication stress-induced chromosomal breaks are also efficiently suppressed by Wnt10b. Thus, our results show that Wnt10b signaling regulates replication stress-induced chromosome missegregation and breakage, and hence, is a determinant for broad genome instability in cancer cells. Summary blurbWe describe a novel role of Wnt10b signaling acting in response to DNA replication stress to suppress chromosomal breaks and mitotic errors in human cancer cells.

cell biology↗