Format

Send to

Choose Destination
Development. 2018 Dec 5;145(23). pii: dev169136. doi: 10.1242/dev.169136.

Fetal Leydig cells dedifferentiate and serve as adult Leydig stem cells.

Author information

1
Department of Anatomy, Kawasaki Medical School, 577 Matsushima, Kurashiki, Okayama 701-0192, Japan yshima@med.kawasaki-m.ac.jp.
2
Department of Molecular Biology, Graduate School of Medical Sciences, Kyushu University, 3-1-1 Maidashi, Higashi-ku, Fukuoka 812-8582, Japan.
3
Department of Systems Life Sciences, Graduate School of Systems Life Sciences and Division of Bioinformatics, Medical Institute of Bioregulation, Kyushu University, 3-1-1 Maidashi, Higashi-ku, Fukuoka 812-8582, Japan.
4
AMED-CREST, Japan Agency for Medical Research and Development, Fukuoka.
5
Department of Systems Life Sciences, Graduate School of Systems Life Sciences and Research Center for Transomics Medicine, Medical Institute of Bioregulation, Kyushu University, 3-1-1 Maidashi, Higashi-ku, Fukuoka 812-8582, Japan.
6
Department of Systems Biology, Graduate School of Pharmaceutical Sciences, Kyoto University, Sakyo-ku, Kyoto 606-8501, Japan.
7
Department of Developmental Genetics, Institute of Advanced Medicine, Wakayama Medical University (WMU), Kimiidera, Wakayama 641-8509, Japan.

Abstract

Previous studies have established that fetal Leydig cells (FLCs) and adult Leydig cells (ALCs) show distinct functional characteristics. However, the lineage relationship between FLCs and ALCs has not been clarified yet. Here, we reveal that a subset of FLCs dedifferentiate at fetal stages to give rise to ALCs at the pubertal stage. Moreover, the dedifferentiated cells contribute to the peritubular myoid cell and vascular pericyte populations in the neonatal testis, and these non-steroidogenic cells serve as potential ALC stem cells. We generated FLC lineage-specific Nr5a1 (Ad4BP/SF-1) gene-disrupted mice and mice lacking the fetal Leydig enhancer (FLE) of the Nr5a1 gene. Phenotypes of these mice support the conclusion that most of the ALCs arise from dedifferentiated FLCs, and that the FLE of the Nr5a1 gene is essential for both initial FLC differentiation and pubertal ALC redifferentiation.

KEYWORDS:

Adult Leydig cell; Dedifferentiation; Fetal Leydig cell; Mouse; Stem cell; Testis

PMID:
30518625
DOI:
10.1242/dev.169136
[Indexed for MEDLINE]
Free full text

Supplemental Content

Full text links

Icon for HighWire
Loading ...
Support Center