原创力文档reprogramming to pluripotency can conceal somatic cell chromosomal instability重组多能性可以掩盖体细胞染色体不稳定.pdfVIP
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reprogramming to pluripotency can conceal somatic cell chromosomal instability重组多能性可以掩盖体细胞染色体不稳定
Reprogramming to Pluripotency Can Conceal Somatic
Cell Chromosomal Instability
1. 1,2. 2 2 1,2
Masakazu Hamada , Liviu A. Malureanu , Tobias Wijshake , Wei Zhou , Jan M. van Deursen *
1 Department of Biochemistry and Molecular Biology, Mayo Clinic, Rochester, Minnesota, United States of America, 2 Department of Pediatric and Adolescent Medicine,
Mayo Clinic, Rochester, Minnesota, United States of America
Abstract
The discovery that somatic cells are reprogrammable to pluripotency by ectopic expression of a small subset of
transcription factors has created great potential for the development of broadly applicable stem-cell-based therapies. One
of the concerns regarding the safe use of induced pluripotent stem cells (iPSCs) in therapeutic applications is loss of
genomic integrity, a hallmark of various human conditions and diseases, including cancer. Structural chromosome defects
such as short telomeres and double-strand breaks are known to limit reprogramming of somatic cells into iPSCs, but
whether defects that cause whole-chromosome instability (W-CIN) preclude reprogramming is unknown. Here we
demonstrate, using aneuploidy-prone mouse embryonic fibroblasts (MEFs) in which chromosome missegregation is driven
by BubR1 or RanBP2 insufficiency, that W-CIN is not a barrier to reprogramming. Unexpectedly, the two W-CIN defects had
contrasting effects on iPSC genomic integrity, with BubR1 hypomorphic MEFs almost exclusively yielding aneuploid iPSC
clones and RanBP2 hypomorphic MEFs karyotypically normal iPSC clones. Moreover, BubR1-insufficient iPSC clones were
karyotypi
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