• Stephanie C Tran, Emily J Jaehne, Laura E Dye, Joanne Wong, Jana S Bakas, Jemma G Gasperoni, Matthew W Hale, Maarten van den Buuse, Sebastian Dworkin, Sylvia V H Grommen, and Bert De Groef.
• Department of Physiology, Anatomy and Microbiology, La Trobe University, Bundoora, Victoria, Australia.
• Neuroscience. 2021 Feb 10; 455: 30-38.

AbstractThe proto-oncogene pleomorphic adenoma gene 1 (Plag1) encodes a zinc finger transcription factor. PLAG1 is part of the high motility group AT hook-2 (HGMA2)-PLAG1-insulin-like growth factor 2 (IGF2) pathway that, when disrupted, leads to Silver-Russell syndrome, a severe form of intrauterine growth restriction. With little known about PLAG1's role in normal physiology, this study is the first to characterise the behavioural phenotype of PLAG1-deficient mice. Mice were tested for differences in circadian locomotor activity and body temperature, sleep-like behaviour, anxiety-like behaviour, cognition, social behaviour, and sensorimotor gating. Overall, the behavioural phenotype of the Plag1 knock-out (KO) mice was mild: no significant differences were seen in circadian activity levels, locomotion, object recognition, spatial memory or sociability compared to wild-type mice. However, the cued test of fear conditioning, prepulse inhibition of the startle response and Preyer's reflex test suggest that Plag1 KO mice may have a hearing impairment. This implies that PLAG1 plays an important role in proper functioning and/or development of the neural circuitry behind the auditory processes or interacts with genes involved in those processes.Copyright © 2020 IBRO. Published by Elsevier Ltd. All rights reserved.

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