Redundant function of RALDH1 and RALDH2 in the seminiferous epithelium
Résumé
The fact that retinoic acid (RA), the active metabolite of vitamin A (or retinol; ROL) is important in testis homeostasis is well documented since decades, but its precise role at different steps of spermatogenesis is still debated1.
RA, synthesized by the retinaldehyde dehydrogenases (RALDH1 to 3), binds to and activates nuclear receptors (RAR) either within the RA-synthesizing cells themselves or within neighboring cells. RALDH1 and RALDH2 are the main RA-synthesizing enzymes expressed in Sertoli cells and germ cells (GC), respectively, while RALDH3 is not detected in the seminiferous epithelium2.
In the past we showed that RALDH-dependent synthesis of RA in the Sertoli cells is instrumental to initiate spermatogonia differentiation and therefore to launch the 1st spermatogenic wave at the onset of puberty3.
Here we evaluated the role of RALDHs in the GC (RaldhGerm−/− mutants).
We have used a combination of cell-type specific genetic ablations and pharmacological approaches in vivo to show that RA synthesis in postpubertal testis relies on both somatic and GC, two sources that are functionally redundant.
Domaines
Reproduction sexuée
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