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Is the primate-specific protein pLG72 affecting SOD1 functionality and superoxide formation?

Giulia Murtas1, Silvia Sacchi1,2, Meenakshi Sundaram Kumar3

  • 1Department of Biotechnology and Life Sciences, University of Insubria, Varese, Italy.

Free Radical Research
|July 7, 2020
PubMed
Summary

Primate protein pLG72 does not affect SOD1 function or aggregation. This study excludes a role for pLG72 in amyotrophic lateral sclerosis (ALS) susceptibility, despite initial hypotheses.

Keywords:
Reactive oxygen species (ROS)amyotrophic lateral sclerosiscopper zinc-superoxide dismutasestresssuperoxide dismutase

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Area of Science:

  • Neuroscience
  • Molecular Biology
  • Cell Biology

Background:

  • pLG72 is a primate-specific protein with unknown function, potentially linked to mitochondria and D-amino acid oxidase (DAAO).
  • DAAO degrades D-serine, and mutations in DAAO are implicated in amyotrophic lateral sclerosis (ALS).
  • Previous studies suggested pLG72 expression in glioblastoma cells reduced proliferation, increased superoxide radicals, and affected SOD1 activity and aggregation.

Purpose of the Study:

  • To investigate the potential link between pLG72 and SOD1, particularly in the context of ALS.
  • To determine if pLG72 modulates SOD1 function, stability, or aggregation.

Main Methods:

  • In vitro studies using recombinant proteins to assess complex formation and SOD1 activity/stability.
  • Cellular studies involving ectopic expression of wild-type and R30K pLG72 variants in U87 glioblastoma cells.
  • Analysis of cell viability, ROS/superoxide production, caspase activity, and SOD1/pLG72 colocalization.

Main Results:

  • In vitro studies showed no stable complex formation between pLG72 and SOD1, nor any effect on SOD1 activity or stability.
  • Cellular expression of pLG72 did not alter cell viability or ROS production; only the R30K variant slightly increased caspase activity.
  • pLG72 and SOD1 did not colocalize within cells, with pLG72 primarily in mitochondria and SOD1 in the cytosol.
  • pLG72 expression did not affect SOD1 expression levels or aggregation.

Conclusions:

  • Biochemical and cellular data exclude a role for pLG72 in modulating SOD1 function and aggregation.
  • pLG72 is unlikely to play a role in amyotrophic lateral sclerosis (ALS) susceptibility.