title: Defending male fertility.
abstract: An estimated 10 to 15% of couples suffer from infertility, and many treatment decisions rely on trial and error. In this issue of Science Translational Medicine, Tollner and colleagues provide strong evidence from a human genetics study that a common variant in the beta defensin 126 gene, the "del" variant, can reduce male fertility substantially. In addition, they show a plausible mechanism for reduced fertility: Sperm from del/del homozygotes lack an important component of their glycoprotein coat and have difficulty penetrating a surrogate for cervical mucus. If replicated in future studies, these findings promise to guide choices about the timing and type of assisted reproduction interventions-and further hint at the possibility of treating sperm from del/del homozygotes to promote fertility.
authors.affiliation: Duke-NUS Graduate Medical School Singapore, 8 College Road, 169857 Singapore. steve.rozen@duke-nus.edu.sg
authors.forename: Steve
authors.initials: S
authors.lastname: Rozen
mesh_terms: D030501:Epididymal Secretory Proteins / Q000235:genetics*; D005260:Female; D006801:Humans; D007248:Infertility, Male / Q000235:genetics* / Q000503:physiopathology*; D008297:Male; D009154:Mutation / Q000235:genetics*; D011247:Pregnancy; D013094:Spermatozoa / Q000473:pathology*; D023083:beta-Defensins
chemical_list: C426184:DEFB126 protein, human; D030501:Epididymal Secretory Proteins; D023083:beta-Defensins