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Determination of Reproductive Competence by Confirming Pubertal Onset and Performing a Fertility Assay in Mice and Rats
Published on: October 13, 2018
Male mice lacking ADAMTS-16 are fertile but exhibit testes of reduced weight
Catherine Livermore1, Nick Warr1, Nicolas Chalon1
1Mammalian Genetics Unit, Medical Research Council, Harwell Institute, Oxfordshire, OX11 0RD, UK.
Abstract:
Adamts16 encodes a disintegrin-like and metalloproteinase with thrombospondin motifs, 16, a member of a family of multi-domain, zinc-binding proteinases. ADAMTS-16 is implicated in a number of pathological conditions, including hypertension, cancer and osteoarthritis. A large number of observations, including a recent report of human ADAMTS16 variants in cases of 46,XY disorders/differences of sex development (DSD), also implicate this gene in human testis determination. We used CRISPR/Cas9 genome editing to generate a loss-of-function allele in the mouse in order to examine whether ADAMTS-16 functions in mouse testis determination or testicular function. Male mice lacking Adamts16 on the C57BL/6N background undergo normal testis determination in the fetal period. However, adult homozygotes have an average testis weight that is around 10% lower than age-matched controls. Cohorts of mutant males tested at 3-months and 6-months of age were fertile. We conclude that ADAMTS-16 is not required for testis determination or male fertility in mice. We discuss these phenotypic data and their significance for our understanding of ADAMTS-16 function.
Insights
ADAMTS-16 is not essential for mouse testis determination or fertility. While adult Adamts16-deficient mice show slightly reduced testis weight, they remain fertile, indicating no critical role in these reproductive functions.
Area of Science:
- Genetics
- Developmental Biology
- Reproductive Science
Background:
- ADAMTS-16 (a disintegrin-like and metalloproteinase with thrombospondin motifs, 16) is a proteinase implicated in various pathologies.
- Human ADAMTS16 variants are linked to 46,XY disorders/differences of sex development (DSD), suggesting a role in human testis determination.
Purpose of the Study:
- To investigate the function of ADAMTS-16 in mouse testis determination and testicular function.
- To generate a loss-of-function mouse model for Adamts16 using CRISPR/Cas9 genome editing.
Main Methods:
- CRISPR/Cas9 genome editing was employed to create Adamts16 loss-of-function mice on a C57BL/6N background.
- Phenotypic analysis, including testis weight assessment and fertility testing, was performed on mutant male mice at different ages.
Main Results:
- Male mice lacking Adamts16 exhibited normal testis determination during the fetal period.
- Adult Adamts16-deficient male mice had approximately 10% lower average testis weight compared to controls.
- Mutant males were fertile at both 3 and 6 months of age.
Conclusions:
- ADAMTS-16 is not required for testis determination in mice.
- ADAMTS-16 is not essential for maintaining male fertility in mice.
- The study provides insights into the function of ADAMTS-16, suggesting its role may not be in primary testis determination or fertility.
