Coding and non-coding roles of MOCCI (C15ORF48) coordinate to regulate host inflammation and immunity

Cheryl Q. E. Lee, Baptiste Kerouanton, Sonia Chothani, Shan Zhang, Ying Chen, Chinmay Kumar Mantri, Daniella Helena Hock, Radiance Lim, Rhea Nadkarni, Vinh Thang Huynh, Daryl Lim, Wei Leong Chew, Franklin L. Zhong, David Arthur Stroud, Sebastian Schafer, Vinay Tergaonkar, Ashley L. John, Owen J. L. Rackham and Lena Ho ()
Additional contact information
Cheryl Q. E. Lee: Institute of Medical Biology, A*STAR
Baptiste Kerouanton: Program in Cardiovascular and Metabolic Disorders
Sonia Chothani: Program in Cardiovascular and Metabolic Disorders
Shan Zhang: Program in Cardiovascular and Metabolic Disorders
Ying Chen: Institute of Molecular and Cell Biology, A*STAR
Chinmay Kumar Mantri: Program in Emerging Infectious Diseases
Daniella Helena Hock: University of Melbourne
Radiance Lim: Program in Cardiovascular and Metabolic Disorders
Rhea Nadkarni: Program in Cardiovascular and Metabolic Disorders
Vinh Thang Huynh: Institute of Molecular and Cell Biology, A*STAR
Daryl Lim: Genome Institute Singapore, A*STAR
Wei Leong Chew: Genome Institute Singapore, A*STAR
Franklin L. Zhong: Nanyang Technological University, Skin Diseases and Wound Repair Program
David Arthur Stroud: University of Melbourne
Sebastian Schafer: Program in Cardiovascular and Metabolic Disorders
Vinay Tergaonkar: Institute of Molecular and Cell Biology, A*STAR
Ashley L. John: Program in Emerging Infectious Diseases
Owen J. L. Rackham: Program in Cardiovascular and Metabolic Disorders
Lena Ho: Institute of Medical Biology, A*STAR

Nature Communications, 2021, vol. 12, issue 1, 1-22

Abstract: Abstract Mito-SEPs are small open reading frame-encoded peptides that localize to the mitochondria to regulate metabolism. Motivated by an intriguing negative association between mito-SEPs and inflammation, here we screen for mito-SEPs that modify inflammatory outcomes and report a mito-SEP named “Modulator of cytochrome C oxidase during Inflammation” (MOCCI) that is upregulated during inflammation and infection to promote host-protective resolution. MOCCI, a paralog of the NDUFA4 subunit of cytochrome C oxidase (Complex IV), replaces NDUFA4 in Complex IV during inflammation to lower mitochondrial membrane potential and reduce ROS production, leading to cyto-protection and dampened immune response. The MOCCI transcript also generates miR-147b, which targets the NDUFA4 mRNA with similar immune dampening effects as MOCCI, but simultaneously enhances RIG-I/MDA-5-mediated viral immunity. Our work uncovers a dual-component pleiotropic regulation of host inflammation and immunity by MOCCI (C15ORF48) for safeguarding the host during infection and inflammation.

Date: 2021
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DOI: 10.1038/s41467-021-22397-5

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