Circular RNA circTmem241 drives group III innate lymphoid cell differentiation via initiation of Elk3 transcription

Nian Liu, Jiacheng He, Dongdong Fan, Yang Gu, Jianyi Wang, Huimu Li, Xiaoxiao Zhu, Ying Du, Yong Tian (), Benyu Liu () and Zusen Fan ()
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Nian Liu: Chinese Academy of Sciences
Jiacheng He: Chinese Academy of Sciences
Dongdong Fan: Chinese Academy of Sciences
Yang Gu: Chinese Academy of Sciences
Jianyi Wang: Chinese Academy of Sciences
Huimu Li: Chinese Academy of Sciences
Xiaoxiao Zhu: Chinese Academy of Sciences
Ying Du: Chinese Academy of Sciences
Yong Tian: University of Chinese Academy of Sciences
Benyu Liu: Zhengzhou University
Zusen Fan: Chinese Academy of Sciences

Nature Communications, 2022, vol. 13, issue 1, 1-14

Abstract: Abstract Innate lymphoid cells (ILCs) exert important roles in host defense, tissue repair and inflammatory diseases. However, how ILC lineage specification is regulated remains largely elusive. Here we identify that circular RNA circTmem241 is highly expressed in group III innate lymphoid cells (ILC3s) and their progenitor cells. CircTmem241 deficiency impairs ILC3 commitment and attenuates anti-bacterial immunity. Mechanistically, circTmem241 interacts with Nono protein to recruit histone methyltransferase Ash1l onto Elk3 promoter in ILC progenitor cells (ILCPs). Ash1l-mediated histone modifications on Elk3 promoter enhance chromatin accessibility to initiate Elk3 transcription. Of note, circTmem241−/−, Nono−/− and Ash1l−/− ILCPs display impaired ILC3 differentiation, while Elk3 overexpression rescues ILC3 commitment ability. Finally, circTmem241−/−Elk3−/− mice show lower numbers of ILC3s and are more susceptible to bacterial infection. We reveal that the circTmem241-Nono-Ash1l-Elk3 axis is required for the ILCP differentiation into ILC3P and ILC3 maturation, which is important to manipulate this axis for ILC development on treatment of infectious diseases.

Date: 2022
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DOI: 10.1038/s41467-022-32322-z

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