Scientists uncover key molecular culprit in ALS: PEG10 gene implicated in pathogenesis ALSResearch Neurodegenerative UBQLN2 PEG10 Retrotransposon GeneExpression AxonRemodeling MotorNeuron eLife
By Dr. Sanchari Sinha Dutta, Ph.D.Jun 7 2023 Scientists at the University of Colorado Boulder, USA, have deciphered molecular mechanisms involved in the pathogenesis of Amyotrophic Lateral Sclerosis . They have identified paternally expressed gene 10 as a significant contributor to disease pathogenesis. Study: UBQLN2 restrains the domesticated retrotransposon PEG10 to maintain neuronal health in ALS.
PEG10 is a domesticated gag-pol retrotransposon that plays crucial roles in placental development and cancer progression. This gene codes for both gag and pol domains separated by a programmed ribosome frameshifting site. To investigate the association between UBQLN2 and PEG10, scientists used human embryonic stem cells lacking UBQLN1, UBQLN2, or UBQLN4 genes and measured the level of PEG10. The findings revealed that only UBQLN2-lacking stem cells have increased accumulation of gag-pol form of PEG10, indicating that PEG10 is an exclusive substrate of UBQLN2.
By tracking self-cleavage-generated protein fragments through confocal microscopy, scientists observed that only nucleocapsid fragment is uniquely localized to the nucleus. RNA sequencing and cluster profiling of differentially expressed genes revealed that upon nuclear translocation, the nucleocapsid fragment induces transcriptional changes similar to that caused by the full-length gag-pol protein.
Paternally expressed gene 10 is enriched in horns of the lumbosacral spinal cord. Tiled image of full-thickness lumbosacral spinal cord section demonstrating Microtubule-associated protein 2 , PEG10, and DAPI staining. Merged image shows outlines of boxes for closer examination in and . Scale bar 1 mm. Merged image of the posterior horn of the spinal cord showing enrichment for both MAP2 and PEG10 signals. Scale bar 200 μm.
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