Supplementary Materials

A Werner syndrome stem cell model unveils heterochromatin alterations as a driver of human aging

Weiqi Zhang, Jingyi Li, Keiichiro Suzuki, Jing Qu, Ping Wang, Junzhi Zhou, Xiaomeng Liu, Ruotong Ren, Xiuling Xu, Alejandro Ocampo, Tingting Yuan, Jiping Yang, Ying Li, Liang Shi, Dee Guan, Huize Pan, Shunlei Duan, Zhichao Ding, Mo Li, Fei Yi, Ruijun Bai, Yayu Wang, Chang Chen, Fuquan Yang, Xiaoyu Li, Zimei Wang, Emi Aizawa, April Goebl, Rupa Devi Soligalla, Pradeep Reddy, Concepcion Rodriguez Esteban, Fuchou Tang, Guang-Hui Liu, Juan Carlos Izpisua Belmonte

Materials/Methods, Supplementary Text, Tables, Figures, and/or References

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  • Materials and Methods
  • Figs. S1 to S11
  • Captions for Tables S1 to S5
  • References (21–47)
Table S1
List of “H3K9me3 mountains” in MSCs-WRN+/+
Table S2
List of differentially expressed genes (fold change, FC [WRN-/- /WRN+/+] > 2 or < 0.5, p<0.05) between WRN-proficient and WRN-deficient ESCs and MSCs.
Table S3
Gene ontology analysis of differentially expressed genes (fold change, FC [MSC-WRN-/- / MSC-WRN+/+] > 2 or < 0.5, p<0.05) between MSCs-WRN+/+ and MSCs-WRN-/-.
Table S4
Information on dental pulp-derived primary MSCs
Table S5
Primers list