scRNA-seq for stromal Lkb1 deficiency-induced gastrointestinal polyps

Numerous studies have showed that mesenchymal-specific Lkb1 is sufficient for the development of PJS-like polyps in mice. However, the cellular origin and component of these Lkb1-associated polyps and underlying mechanisms remain elusive. In this present study, we generated tamoxifen-inducible Lkb1flox/flox;Myh11-Cre/ERT2 mice and performed scRNA-seq to investigate the cellular complexity of gastrointestinal polyps associated with PJS. Overall design: Polyps tissues from three Lkb1flox/+;Myh11-Cre/ERT2 mice and normal duodenum tissues of three Lkb1+/+;Myh11-Cre/ERT2 (WT) mice were collected.

大量研究已证实，在小鼠体内，间质特异性的肝激酶B1（Liver kinase B1, Lkb1）足以诱发色素沉着息肉综合征（Peutz-Jeghers Syndrome, PJS）样息肉的形成。然而，此类与Lkb1相关的息肉的细胞起源、组成成分及其潜在作用机制仍不明晰。本研究构建了他莫昔芬诱导型Lkb1条件性敲除小鼠（Lkb1flox/flox;Myh11-Cre/ERT2），并通过单细胞RNA测序（single-cell RNA sequencing, scRNA-seq）探究了与PJS相关的胃肠道息肉的细胞复杂性。实验设计概述：收集3只Lkb1flox/+;Myh11-Cre/ERT2小鼠的息肉组织，以及3只野生型对照小鼠（Lkb1+/+;Myh11-Cre/ERT2，WT）的正常十二指肠组织。