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Identifying putative substrates of Calpain-15 in neurodevelopment.

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Calpain 15 (CAPN15) deficiency causes developmental eye and brain anomalies. This study used proteomics to identify CAPN15 substrates, finding Doublecortin and Tubb3 were more abundant in its absence.

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Area of Science:

  • Biochemistry
  • Developmental Biology
  • Genetics

Background:

  • Calpain 15 (CAPN15) is a protease in the small optic lobe (SOL) calpain family, crucial for development.
  • CAPN15 loss in mice and humans results in eye anomalies, brain changes, and neurodevelopmental disorders.
  • The specific substrates targeted by CAPN15 remain unknown.

Purpose of the Study:

  • To identify the substrates of Calpain 15 (CAPN15) using proteomic approaches.
  • To investigate the functional consequences of CAPN15 loss on protein expression and cleavage patterns.

Main Methods:

  • Utilized Capn15 knockout (KO) P2 mice for experiments.
  • Employed RNA sequencing (RNA-SEQ), proteomics, and N-terminomics (TAILS) to analyze protein changes.
  • Examined cleavage preferences and substrate abundance in Capn15-/- versus wild-type (WT) mice.

Main Results:

  • Transcriptome analysis revealed minimal changes, with Pax2 transcription factor showing increased levels upon CAPN15 loss.
  • TAILS identified a preference for cleavage at basic residues.
  • Proteomic analysis indicated increased abundance of Doublecortin and Tubb3 in Capn15 KO mice, with predicted cleavage at lysine residues.

Conclusions:

  • CAPN15 plays a role in regulating protein levels, potentially through cleavage at specific residues.
  • While direct substrates were not definitively identified, changes in Doublecortin and Tubb3 abundance suggest their regulation by CAPN15.
  • Further research is needed to fully elucidate CAPN15's substrate repertoire and its precise role in neurodevelopment.