Evidence map›Paper›PMID 42711850›Full record

ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2026

Phase Separation of SF3B1 Serves as a Critical Post-Transcriptional Regulator During Early Mouse Embryogenesis.

Kang Zhao, Ting-Yu Han, Yan-Li Cheng, Yi-Dan Zhang, Yu-Wei Zhang, JinJian Guo, ShaoJun Zhang, WenZe Huang, Jing Zhang, Pei-Yu Liao and 6 more

Abstract read
In one paragraph

Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

16 authors.

Kang Zhao *Department of Biochemistry and Molecular Biology, Shanxi Key Laboratory of Birth Defect and Cell Regeneration, Shanxi Medical University, Taiyuan, China.ORCID https://orcid.org/0000-0001-5621-3564
Ting-Yu Han *Department of Biochemistry and Molecular Biology, Shanxi Key Laboratory of Birth Defect and Cell Regeneration, Shanxi Medical University, Taiyuan, China.ORCID https://orcid.org/0000-0002-7110-8321
Yan-Li Cheng *School of Life Science, Shanxi Normal University, Taiyuan, China.ORCID https://orcid.org/0000-0002-1816-8640
Yi-Dan Zhang *Department of Biochemistry and Molecular Biology, Shanxi Key Laboratory of Birth Defect and Cell Regeneration, Shanxi Medical University, Taiyuan, China.
Yu-Wei Zhang *Guangzhou Key Laboratory of Metabolic Diseases and Reproductive Health, Guangdong-Hong Kong Metabolism & Reproduction Joint Laboratory, Reproductive Medicine Center, Guangdong Second Provincial General Hospital of Jinan University, Guangzhou, China.
JinJian GuoSchool of Life Science, Shanxi Normal University, Taiyuan, China.
ShaoJun ZhangBeijing Advanced Innovation Center for Structural Biology & Frontier Research Center for Biological Structure, School of Life Sciences, Tsinghua University, Beijing, China.ORCID https://orcid.org/0000-0002-6757-3263
WenZe HuangBeijing Advanced Innovation Center for Structural Biology & Frontier Research Center for Biological Structure, School of Life Sciences, Tsinghua University, Beijing, China.ORCID https://orcid.org/0009-0009-6597-7190
Jing ZhangDepartment of Biochemistry and Molecular Biology, Shanxi Key Laboratory of Birth Defect and Cell Regeneration, Shanxi Medical University, Taiyuan, China.
Pei-Yu LiaoThe Second School of Clinical Medicine, Southern Medical University, Guangzhou, China.
Ying XinDepartment of Biochemistry and Molecular Biology, Shanxi Key Laboratory of Birth Defect and Cell Regeneration, Shanxi Medical University, Taiyuan, China.ORCID https://orcid.org/0009-0002-7484-2262
ChuanChen ChuDepartment of Biochemistry and Molecular Biology, Shanxi Key Laboratory of Birth Defect and Cell Regeneration, Shanxi Medical University, Taiyuan, China.
Qing-Yuan SunGuangzhou Key Laboratory of Metabolic Diseases and Reproductive Health, Guangdong-Hong Kong Metabolism & Reproduction Joint Laboratory, Reproductive Medicine Center, Guangdong Second Provincial General Hospital of Jinan University, Guangzhou, China.ORCID https://orcid.org/0000-0002-0148-2414
ZhiZhen LiuDepartment of Biochemistry and Molecular Biology, Shanxi Key Laboratory of Birth Defect and Cell Regeneration, Shanxi Medical University, Taiyuan, China.
Xiang-Hong OuGuangzhou Key Laboratory of Metabolic Diseases and Reproductive Health, Guangdong-Hong Kong Metabolism & Reproduction Joint Laboratory, Reproductive Medicine Center, Guangdong Second Provincial General Hospital of Jinan University, Guangzhou, China.
Jun XieDepartment of Biochemistry and Molecular Biology, Shanxi Key Laboratory of Birth Defect and Cell Regeneration, Shanxi Medical University, Taiyuan, China.ORCID https://orcid.org/0000-0002-6161-5696

Funding

National Natural Science Foundation of China 32300580National Natural Science Foundation of China 32370641National Natural Science Foundation of China U23A20420
6 · The paper itself

Abstract

During early mammalian embryogenesis, totipotent zygotes and early blastomeres undergo extensive post-transcriptional regulation during the establishment of the first cell lineages; however, the functional contribution of alternative splicing to embryonic compaction and blastulation remains poorly understood. Here, we show that SF3B1, a core component of the spliceosome, is upregulated from the 4-cell stage and mediates highly dynamic splicing programs. Depletion of SF3B1 results in developmental arrest at the morula stage, accompanied by widespread transcriptomic dysregulation characterized by aberrant expression of transcription factors that impede pluripotency transition. Alternative splicing analysis further identifies that aberrantly spliced transcripts were significantly enriched in genes involved in cell cycle regulation, such as Cdk11b and Ccnb1. Importantly, we demonstrate that SF3B1 undergoes intrinsic, IDR-driven liquid-liquid phase separation both in vitro and in vivo, forming nuclear condensates in oocytes and early embryos, which is essential for successful development to the blastocyst stage. Together, our findings reveal that phase separation mediated SF3B1 splicing activity is a critical regulator of early mouse embryonic development.

Indexed as

alternative splicingbiologyblastocystcell biologyembryonic stem cellregulatorrna splicingspliceosomesplicing factortranscription factor

Identifiers

PMID42711850
PMCPMC13554399

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.