Kinesin binding as a shared pathway underlying the genetic basis of male factor infertility and insomnia

Abstract

Objective

To study whether male factor infertility and insomnia share genetic risk variants and identify any molecular, cellular, and biologic interactions between these traits.

Design

The in silico study was performed. Two lists of genetic variants were manually curated through a literature review, one of those associated with male factor infertility and the other with insomnia. Genes were assigned to these variants to compose male factor infertility–associated (454 genes) and insomnia-associated (921 genes) gene lists.

Setting

Not applicable.

Patient(s)

Not applicable.

Intervention(s)

Not applicable.

Main Outcome Measure(s)

Enrichment of biologic pathways and protein-protein interaction analysis.

Result(s)

Twenty-eight genes were common to both lists, representing a greater overlap than would be expected by chance. In the 28 genes contained in the intersection list, there was a significant enrichment of pathways related to kinesin binding. A protein-protein interaction analysis using the intersection list as input retrieved 25 nodes and indicated that two of them were kinesin-related proteins (PLEKHM2 and KCL1).

Conclusion(s)

The shared male factor infertility and insomnia genes, and the biologic pathways highlighted in this study, suggest that further functional investigations into the interplay between fertility and sleep are warranted.