Knockdown of Sucla2 decreases the viability of mouse spermatocytes by inducing apoptosis through injury of the mitochondrial function of cells | Zendy

Shaoping Huang | Zendy; Jing Wang | Zendy; Lei Wang | Zendy

Open Access

Knockdown of Sucla2 decreases the viability of mouse spermatocytes by inducing apoptosis through injury of the mitochondrial function of cells

Author(s) -

Shaoping Huang,

Jing Wang,

Lei Wang

Publication year - 2016

Publication title -

folia histochemica et cytobiologica

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 0.384

H-Index - 40

eISSN - 1897-5631

pISSN - 0239-8508

DOI - 10.5603/fhc.a2016.0020

Subject(s) - gene knockdown , spermatogenesis , spermatocyte , biology , apoptosis , viability assay , flow cytometry , transfection , microbiology and biotechnology , cell culture , endocrinology , biochemistry , gene , genetics , meiosis

Sucla2, a β subunit of succinyl coenzyme A synthase, is located in the mitochondrial matrix. Sucla2 catalyzes the reversible synthesis of succinate and adenosine triphosphate (ATP) in the tricarboxylic acid cycle. Sucla2 expression was found to be correlated with the capacitation of boar spermatozoa. We have previously reported that Sucla2 was decreased in the testes of rats with spermatogenesis failure after exposure to endocrine disruptor BDE47. Yet, the expression model of Sucla2 in spermatogenesis and the function of Sucla2 in spermatogenic cells are still unclear. Our objective was to explore the localization of Sucla2 during mouse spermatogenesis and its function in the mouse spermatocyte line (GC2).

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