# EMC3 deletion in mouse liver and fat impairs triglyceride storage; FITM2 identified as EMC client

- Published: 2026-11-05 03:32 UTC
- Section: Life & Health › Biology & biochemistry
- Tags: ER membrane complex, EMC3 deletion, FITM2 EMC client, lipid droplet biogenesis, triglyceride storage, non-shivering thermogenesis, adipose tissue mice, Drosophila fat body, lipid homeostasis
- URL: https://realtech.media/news/rt-71cdd78bedebce136a6c3a98_emc3_deletion_in/

**Portuguese and UK groups deleted the EMC3 subunit in mouse and Drosophila tissues. Lipid droplet homeostasis was disrupted and levels of the protein FITM2 fell.**

![EMC3 deletion in mouse liver and fat impairs triglyceride storage; FITM2 identified as EMC client](https://sgzwpqqelzmajkcubgkl.supabase.co/storage/v1/object/public/rt-media/2026/11/d807dd816a070fe5.jpg)
*Sinkevichvictoria, Wikimedia Commons, CC BY 4.0*

A team from the Gulbenkian Institute for Molecular Medicine and ITQB NOVA (Oeiras, Portugal), the University of Oxford and Queen's University Belfast reported in Nature Communications, published on 3 November 2026, that the ER membrane complex (EMC) is needed for normal triglyceride storage in mice and in Drosophila. [1] The EMC inserts integral membrane proteins into the lipid bilayer of the endoplasmic reticulum (ER). [1] Its structure has been studied in detail in recent years, but which proteins depend on it and what it does across evolution remained less well understood, the authors write. [1]

## Tissue-specific EMC3 deletion in mice

The researchers deleted the essential EMC3 subunit in the liver and in adipose tissues of mice. They then examined the animals in a range of metabolic and lipid homeostasis models. [1]

Loss of EMC3 in either the liver or adipose tissue led to defective storage of triglycerides and disturbed lipid droplet (LD) homeostasis. [1] Adipose tissue lacking EMC was less able to mediate fat storage in mice on a high-fat diet. It was also unable to support non-shivering thermogenesis. [1]

## FITM2 as an EMC client

Proteomic analysis of EMC3-deficient tissues showed reduced levels of FITM2, a key regulator of LD biogenesis and ER homeostasis. On this basis the authors identify FITM2 as an EMC client. [1]

The team then deleted EMC3 in the fat body of Drosophila, which produced similar defects in LD homeostasis. These defects were rescued by a FITM2 mutant whose biogenesis does not depend on the EMC. [1]

The authors conclude that the EMC plays a key, evolutionarily conserved role in the biogenesis of the machinery that maintains triglyceride storage in metazoans. [1] The data come from mouse and fly models. The corresponding authors are John C. Christianson, Pedro M. Domingos and Colin Adrain. [1]

## Sources

1. [Nature Communications](https://doi.org/10.1038/s41467-026-78684-6)

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Source: RealTech, realtech.media — https://realtech.media/news/rt-71cdd78bedebce136a6c3a98_emc3_deletion_in/