2. Academic Validation
  3. NECL2 regulates blood-testis barrier dynamics in mouse testes

NECL2 regulates blood-testis barrier dynamics in mouse testes

  • Cell Tissue Res. 2023 Mar 6. doi: 10.1007/s00441-023-03759-5.
Jun Fu 1,  Xiao Liu 2,  Bin Yin 2,  Pengcheng Shu 2,  Xiaozhong Peng 3 4
Affiliations

Affiliations

  • 1 National Demonstration Center for Experimental Basic Medical Education, and State Key Laboratory of Medical Molecular Biology, Institute of Basic Medical Sciences Chinese Academy of Medical Sciences, School of Basic Medicine Peking Union Medical College, Beijing, 100005, China.
  • 2 State Key Laboratory of Medical Molecular Biology, and Department of Molecular Biology and Biochemistry, Institute of Basic Medical Sciences Chinese Academy of Medical Sciences, School of Basic Medicine Peking Union Medical College, No. 5, Dongdan Santiao, Dongcheng District, Beijing, 100005, China.
  • 3 National Demonstration Center for Experimental Basic Medical Education, and State Key Laboratory of Medical Molecular Biology, Institute of Basic Medical Sciences Chinese Academy of Medical Sciences, School of Basic Medicine Peking Union Medical College, Beijing, 100005, China. pengxiaozhong@pumc.edu.cn.
  • 4 State Key Laboratory of Medical Molecular Biology, and Department of Molecular Biology and Biochemistry, Institute of Basic Medical Sciences Chinese Academy of Medical Sciences, School of Basic Medicine Peking Union Medical College, No. 5, Dongdan Santiao, Dongcheng District, Beijing, 100005, China. pengxiaozhong@pumc.edu.cn.
PMID: 36872374 DOI: 10.1007/s00441-023-03759-5
Abstract

The adhesion protein nectin-like molecule 2 (NECL2) is involved in spermatogenesis and participates in the connections between Sertoli cells and germ cells. Necl2 deficiency leads to infertility in male mice. We found that NECL2 is relatively highly expressed on the cell membranes of preleptotene spermatocytes. It is known that preleptotene spermatocytes pass through the blood-testis barrier (BTB) from the base of the seminiferous tubules to the lumen to complete meiosis. We hypothesized that the NECL2 protein on the surfaces of preleptotene spermatocytes has an effect on the BTB when crossing the barrier. Our results showed that Necl2 deficiency caused the levels of proteins in the BTB to be abnormal, such as those of Claudin 3, claudin 11, and Connexin43. NECL2 interacted and colocalized with adhesion proteins forming the BTB, such as Connexin43, Occludin, and N-Cadherin. NECL2 regulated BTB dynamics when preleptotene spermatocytes passed through the barrier, and Necl2 deficiency caused BTB damage. Necl2 deletion significantly affected the testicular transcriptome, especially the expression of spermatogenesis-related genes. These results suggest that before meiosis and spermatid development occur, BTB dynamics regulated by NECL2 are necessary for spermatogenesis.

Keywords

Adhesion protein; Blood-testis barrier; Nectin-like molecule 2; Spermatogenesis; Spermatogenic failure.

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