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Defective Wnt3 expression by testicular Sertoli cells compromise male fertility

  • Basu, Sayon1
  • Arya, Satya Pal1, 2
  • Usmani, Abul1, 3
  • Pradhan, Bhola Shankar1, 4
  • Sarkar, Rajesh Kumar1
  • Ganguli, Nirmalya1, 2
  • Shukla, Mansi1
  • Mandal, Kamal1
  • Singh, Surendra5
  • Sarda, Kanchan1, 6
  • Majumdar, Subeer S.1, 2, 5
  • 1 National Institute of Immunology, Cellular Endocrinology Laboratory, New Delhi, Delhi, 110067, India , New Delhi (India)
  • 2 National Institute of Animal Biotechnology, Hyderabad, India , Hyderabad (India)
  • 3 Washington University School of Medicine, Department of Genetics, St. Louis, MO, USA , St. Louis (United States)
  • 4 Nencki Institute of Experimental Biology PAS, Laboratory of Synaptogenesis, Ludwik Pasteur 3 street, Warsaw, 02-093, Poland , Warsaw (Poland)
  • 5 National Institute of Immunology, Primate Research Center, New Delhi, Delhi, India , New Delhi (India)
  • 6 Indian Spinal Injuries Centre, Research Department, New Delhi, India , New Delhi (India)
Published Article
Cell and Tissue Research
Publication Date
Oct 24, 2017
DOI: 10.1007/s00441-017-2698-5
Springer Nature


Testicular Sertoli cells make a niche for the division and differentiation of germ cells. Sertoli cells respond to increased follicle-stimulating hormone (FSH) and testosterone (T) levels at the onset of puberty by producing paracrine factors which affect germ cells and trigger robust onset of spermatogenesis. Such paracrine support to germ cells is absent during infancy, despite Sertoli cells being exposed to high FSH and T within the infant testis. This situation is similar to certain cases of male idiopathic infertility where post-pubertal Sertoli cells fail to support germ cell division and differentiation in spite of endogenous or exogenous hormonal support. Defective Sertoli cells in such individuals may fail to express the full complement of their paracrine repertoire. Identification and supplementation with such factors may overcome Sertoli cells deficiencies and help trigger quantitatively and qualitatively normal differentiation of germ cells. To this end, we compared the transcriptome of FSH- and T-treated infant and pubertal monkey Sertoli cells by DNA microarray. Expression of Wnt3, a morphogen of the Wnt/β-catenin pathway, was higher in pubertal Sertoli cells relative to infant Sertoli cells. Transgenic mice were generated by us in which Wnt3 expression was curtailed specifically in post-pubertal Sertoli cells by shRNA. Subfertility and oligozoospermia were noticed in such animals with low Wnt3 expression in post-pubertal Sertoli cells along with diminished expression of Connexin43, a gap-junctional molecule essential for germ cell development. We report that the FSH- and T-targetedf Wnt3 governs Sertoli cell-mediated regulation of spermatogenesis and hence is crucial for fertility.

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