Established whether CATSPERδ is functionally required for the sperm Ca²⁺ channel, answering how loss of this subunit affects channel activity and fertility.
Evidence Tmem146 knockout mouse with sperm electrophysiology, motility analysis, and localization studies
- Does not resolve whether CATSPERδ acts in channel assembly versus membrane trafficking
- No structural model of how CATSPERδ integrates into the CATSPER complex
- Direct binding partners within the complex not biochemically mapped