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Deletion of Gpatch2 does not alter Tnf expression in mice.

Destiny Dalseno^1,2, Holly Anderton^1,2, Andrew Kueh^1,2

¹The Walter and Eliza Hall Institute of Medical Research, Parkville, VIC, 3052, Australia.

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|March 27, 2023

Summary

GPATCH2 does not regulate tumor necrosis factor (TNF) expression in vivo. Studies in Gpatch2 knockout mice found no effect on basal or inflammation-induced TNF levels, suggesting no role in immune response regulation.

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Area of Science:

Immunology
Molecular Biology
Genetics

Background:

Tumor necrosis factor (TNF) is crucial for immune defense but its dysregulation causes inflammatory diseases.
Controlling TNF levels is vital for immune homeostasis and overall health.
GPATCH2 was identified as a potential post-transcriptional repressor of TNF via its 3' UTR.

Purpose of the Study:

To investigate the in vivo role of GPATCH2 in regulating TNF expression.
To characterize the phenotype of Gpatch2 knockout mice.

Main Methods:

CRISPR screening to identify TNF regulators.
Generation and analysis of Gpatch2 knockout (Gpatch2-/-) mice on a C57BL/6 background.
Assessment of basal and inflammation-induced TNF expression (LPS and SMAC-mimetic models).
Histological examination of tissues and blood cell composition analysis.

Main Results:

GPATCH2 protein was detected in mouse testis and other tissues.
Gpatch2-/- mice exhibited normal basal and inflammation-induced TNF expression.
No significant morphological abnormalities were observed in Gpatch2-/- mice, including lymphoid tissues.
Gpatch2-/- mice were viable and grossly normal with no notable aberrations in blood cell counts.

Conclusions:

GPATCH2 does not appear to play a discernible role in regulating TNF expression in vivo.
The absence of an overt phenotype in Gpatch2-/- mice suggests further investigation is needed to elucidate GPATCH2's function.
The proposed role of GPATCH2 as a TNF repressor requires re-evaluation based on these findings.