Evidence map›Paper›PMID 41723267›Full record

ArticleCommunications biology2026

Single-nucleus multi-omics analysis of mouse small-intestinal Lgr5+ cell populations reveals Foxa3-induced Paneth cell-lineage differentiation.

Xinran Deng, Shenfei Sun, Chenqi Lu, Hanxiao Du, Xiaoyu You, Fujing Huang, Kai Gong, Jingxin Guo, Yumou Gong, Runrong Li and 4 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Communications biology, 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

14 authors.

Xinran Deng *State Key Laboratory of Genetics and Development of Complex Phenotypes, Greater Bay Area Institute of Precision Medicine (Guangzhou), School of Life Sciences, Fudan University, Shanghai, China.ORCID http://orcid.org/0009-0005-7371-3444
Shenfei Sun *State Key Laboratory of Genetics and Development of Complex Phenotypes, Greater Bay Area Institute of Precision Medicine (Guangzhou), School of Life Sciences, Fudan University, Shanghai, China.ORCID http://orcid.org/0000-0002-5034-4333
Chenqi Lu *State Key Laboratory of Genetics and Development of Complex Phenotypes, Greater Bay Area Institute of Precision Medicine (Guangzhou), School of Life Sciences, Fudan University, Shanghai, China.
Hanxiao DuState Key Laboratory of Genetics and Development of Complex Phenotypes, Greater Bay Area Institute of Precision Medicine (Guangzhou), School of Life Sciences, Fudan University, Shanghai, China.
Xiaoyu YouState Key Laboratory of Genetics and Development of Complex Phenotypes, Greater Bay Area Institute of Precision Medicine (Guangzhou), School of Life Sciences, Fudan University, Shanghai, China.
Fujing HuangState Key Laboratory of Genetics and Development of Complex Phenotypes, Greater Bay Area Institute of Precision Medicine (Guangzhou), School of Life Sciences, Fudan University, Shanghai, China.
Kai GongState Key Laboratory of Genetics and Development of Complex Phenotypes, Greater Bay Area Institute of Precision Medicine (Guangzhou), School of Life Sciences, Fudan University, Shanghai, China.
Jingxin GuoShanghai Sci-Tech Inno Center for Infection & Immunity, Shanghai, China.
Yumou GongState Key Laboratory of Genetics and Development of Complex Phenotypes, Greater Bay Area Institute of Precision Medicine (Guangzhou), School of Life Sciences, Fudan University, Shanghai, China.
Runrong LiState Key Laboratory of Genetics and Development of Complex Phenotypes, Greater Bay Area Institute of Precision Medicine (Guangzhou), School of Life Sciences, Fudan University, Shanghai, China.
Xingyu YuState Key Laboratory of Genetics and Development of Complex Phenotypes, Greater Bay Area Institute of Precision Medicine (Guangzhou), School of Life Sciences, Fudan University, Shanghai, China.
Bing ZhaoState Key Laboratory of Genetics and Development of Complex Phenotypes, Greater Bay Area Institute of Precision Medicine (Guangzhou), School of Life Sciences, Fudan University, Shanghai, China. bingzhao@fudan.edu.cn.ORCID http://orcid.org/0000-0001-9891-3569
Xinhua LinState Key Laboratory of Genetics and Development of Complex Phenotypes, Greater Bay Area Institute of Precision Medicine (Guangzhou), School of Life Sciences, Fudan University, Shanghai, China. xlin@fudan.edu.cn.ORCID http://orcid.org/0000-0002-1063-749X
Ning JiangState Key Laboratory of Genetics and Development of Complex Phenotypes, Greater Bay Area Institute of Precision Medicine (Guangzhou), School of Life Sciences, Fudan University, Shanghai, China. ningjiang@fudan.edu.cn.ORCID http://orcid.org/0000-0003-0664-6286

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Lgr5+ stem cells play crucial roles in maintaining intestinal epithelial cell homeostasis. However, the cellular heterogeneity and underlying regulatory programs of Lgr5+ small intestinal stem cells (ISCs) remain elusive. In this study, we profiled gene expression and chromatin accessibility of Lgr5+ ISCs at single-cell resolution to gain a deeper understanding of the lineage specification and early fate determining mechanisms. Our analysis identified a total of 6 subsets of Lgr5+ cell populations, which exhibited heterogeneity in gene expression and chromatin structure. We found that early fate-determining processes diverged the absorptive and secretory lineages within Lgr5+ cells. We further constructed gene regulatory networks controlling lineage determination and identified Foxa3 as a key transcription factor that regulates the differentiation of the intestinal secretory precursor. In vitro knockdown of Foxa3 disrupted the differentiation of Paneth cells by modulating Peroxisome-Proliferator-Activated Receptors (PPARs). Further Foxa3-targeted CUT&Tag sequencing analysis also verified that Foxa3 predominantly drives Paneth cell differentiation in the small intestine by regulating the expression of core genes in the PPAR signaling pathway. These results provide a comprehensive reference map for advancing our understanding of intestinal epithelial development and related diseases.

Indexed as

Cell DifferentiationCell LineageHepatocyte Nuclear Factor 3-gammaIntestine, SmallPaneth CellsReceptors, G-Protein-CoupledAnimalsGene Regulatory NetworksMiceMultiomicsSignal TransductionStem CellsFoxa3 protein, mouseHepatocyte Nuclear Factor 3-gammaLgr5 protein, mouseReceptors, G-Protein-Coupled

Identifiers

PMID41723267
PMCPMC13035940

What OpenQuestion holds

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Registered trials

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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.