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H1FOO-DD 提高了重编程为原始多能性的效率和均匀性。

H1FOO-DD promotes efficiency and uniformity in reprogramming to naive pluripotency.

机构信息

Center for iPS Cell Research and Application (CiRA), Kyoto University, Kyoto 606-8507, Japan; Gladstone Institute of Cardiovascular Disease, San Francisco, CA 94158, USA.

Center for iPS Cell Research and Application (CiRA), Kyoto University, Kyoto 606-8507, Japan; CiRA Foundation, Kyoto 606-8397, Japan.

出版信息

Stem Cell Reports. 2024 May 14;19(5):710-728. doi: 10.1016/j.stemcr.2024.04.005. Epub 2024 May 2.

DOI:10.1016/j.stemcr.2024.04.005
PMID:38701780
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11103934/
Abstract

Heterogeneity among both primed and naive pluripotent stem cell lines remains a major unresolved problem. Here we show that expressing the maternal-specific linker histone H1FOO fused to a destabilizing domain (H1FOO-DD), together with OCT4, SOX2, KLF4, and LMYC, in human somatic cells improves the quality of reprogramming to both primed and naive pluripotency. H1FOO-DD expression was associated with altered chromatin accessibility around pluripotency genes and with suppression of the innate immune response. Notably, H1FOO-DD generates naive induced pluripotent stem cells with lower variation in transcriptome and methylome among clones and a more uniform and superior differentiation potency. Furthermore, we elucidated that upregulation of FKBP1A, driven by these five factors, plays a key role in H1FOO-DD-mediated reprogramming.

摘要

在已分化和未分化的多能干细胞系中，异质性仍然是一个未解决的主要问题。在这里，我们表明，在人类体细胞中表达与母体特异性连接组蛋白 H1FOO 融合的不稳定结构域（H1FOO-DD），与 OCT4、SOX2、KLF4 和 LMYC 一起，可提高向已分化和未分化多能性的重编程质量。H1FOO-DD 的表达与多能性基因周围染色质可及性的改变以及固有免疫反应的抑制有关。值得注意的是，H1FOO-DD 产生的幼稚诱导多能干细胞在克隆间具有更低的转录组和甲基组变异性，以及更均匀和优越的分化能力。此外，我们阐明了由这五个因素驱动的 FKBP1A 的上调在 H1FOO-DD 介导的重编程中起着关键作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2643/11103934/89d856c88053/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2643/11103934/57408329aa3d/fx1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2643/11103934/f9c53c9b129d/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2643/11103934/553f816e433f/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2643/11103934/e64a1e85d01b/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2643/11103934/51e44a4a920e/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2643/11103934/a5384ff12db5/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2643/11103934/89d856c88053/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2643/11103934/57408329aa3d/fx1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2643/11103934/f9c53c9b129d/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2643/11103934/553f816e433f/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2643/11103934/e64a1e85d01b/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2643/11103934/51e44a4a920e/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2643/11103934/a5384ff12db5/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2643/11103934/89d856c88053/gr6.jpg

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