Propagation of paternal sperm-contributed mitochondrial genes, resulting in heteroplasmy, is seldom observed in mammals due to post-fertilization degradation of sperm mitochondria, referred to as sperm mitophagy. Whole organelle sperm mitochondrion degradation is thought to be mediated by the interplay between the ubiquitin-proteasome system (UPS) and the autophagic pathway (Song et al., Proc. Natl. Acad. Sci. USA, 2016). Both porcine and primate post-fertilization sperm mitophagy rely on the ubiquitin-binding autophagy receptor, sequestosome 1 (SQSTM1), and the proteasome-interacting ubiquitinated protein dislocase, valosin-containing protein (VCP). Consequently, we anticipated that sperm mitophagy could be reconstituted in a cell-free system consisting of permeabilized mammalian spermatozoa co-incubated with porcine oocyte extracts. We found that SQSTM1 was detected in the midpiece/mitochondrial sheath of the sperm tail after, but not before, co-incubation with oocyte extracts. VCP was prominent in the sperm mitochondrial sheath both before and after the extract co-incubation and was also detected in the acrosome and postacrosomal sheath and the subacrosomal layer of the spermatozoa co-incubated with extraction buffer as control. Such patterns are consistent with our previous observation of SQSTM1 and VCP associating with sperm mitochondria inside the porcine zygote. In addition, it was observed that sperm head expansion mimicked the early stages of paternal pronucleus development in a zygote during prolonged sperm-oocyte extract co-incubation. Treatment with anti-SQSTM1 antibody during extract co-incubation prevented ooplasmic SQSTM1 binding to sperm mitochondria. Even in an interspecific cellular environment encompassing bull spermatozoa and porcine oocyte extract, ooplasmic SQSTM1 was recruited to heterospecific sperm mitochondria. Complementary with the binding of SQSTM1 and VCP to sperm mitochondria, two sperm-borne pro-mitophagy proteins, parkin co-regulated gene product (PACRG) and spermatogenesis associated 18 (SPATA18), underwent localization changes after extract coincubation, which were consistent with their degradation observed inside fertilized porcine oocytes. These results demonstrate that the early developmental events of post-fertilization sperm mitophagy observed in porcine zygote can be reconstituted in a cell-free system, which could become a useful tool for identifying additional molecules that regulate mitochondrial inheritance in mammals.

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8466530PMC
http://dx.doi.org/10.3390/cells10092450DOI Listing

Publication Analysis

Top Keywords

sperm mitophagy
20
sperm mitochondria
20
sperm
14
cell-free system
12
post-fertilization sperm
12
extract co-incubation
12
events post-fertilization
8
reconstituted cell-free
8
spermatozoa co-incubated
8
porcine oocyte
8

Similar Publications

Study on the role of mitophagy and pyroptosis induced by nano-silver in testicular injury.

Food Chem Toxicol

January 2025

School of Public Health, Zunyi Medical University, Zunyi, Guizhou, 563000, PR China; Key Laboratory of Maternal & Child Health and Exposure Science of Guizhou Higher Education Institutes, Zunyi, Guizhou, 563000, PR China. Electronic address:

Silver nanoparticles(AgNPs)have been widely used in biomedicine and industry. Growing studies have shown that AgNPs can induce sperm motility decrease and spermiogenesis disorders. In this study, animal experiments were used to investigate the role of mitophagy and pyroptosis caused by AgNPs (25.

View Article and Find Full Text PDF

Comparison of different processed products of for the treatment of mice asthenozoospermia.

Transl Androl Urol

October 2024

Key Laboratory of Basic Pharmacology of Guizhou Province and School of Pharmacy, Zunyi Medical University, Zunyi, China.

Article Synopsis
  • GZP, a co-processed mixture with salt and wine, effectively treats asthenozoospermia (reduced sperm motility) in mice by enhancing sexual function and testicular health.
  • The study involved establishing a mouse model for the condition and testing six products, revealing GZP significantly improves sperm count, survival, and reduces deformities.
  • GZP appears to work by inhibiting excessive mitophagy and maintaining mitochondrial integrity, reducing harmful reactive oxygen species (ROS), and blocking certain protein expressions related to cell death.
View Article and Find Full Text PDF

Contribution of impaired autophagy, mitochondrial dysfunction and abnormal lipolysis to epididymal aging in mice.

Exp Gerontol

October 2024

Department of Histology & Embryology, School of Basic Medical Sciences, Anhui Medical University, Hefei 230032, China. Electronic address:

With the increase of the aged population in modern society, research on aging and aging-related diseases has attracted increasing attention. Unlike women, men experience changes gradually in the reproductive system during aging. The epididymis is an important organ for sperm maturation and storage, but less study has been conducted to investigate cellular senescence in aging epididymis and the corresponding influences on sperm.

View Article and Find Full Text PDF

Mitochondria are maternally inherited, but the mechanisms underlying paternal mitochondrial elimination after fertilization are far less clear. Using Drosophila, we show that special egg-derived multivesicular body vesicles promote paternal mitochondrial elimination by activating an LC3-associated phagocytosis-like pathway, a cellular defense pathway commonly employed against invading microbes. Upon fertilization, these egg-derived vesicles form extended vesicular sheaths around the sperm flagellum, promoting degradation of the sperm mitochondrial derivative and plasma membrane.

View Article and Find Full Text PDF

The mitophagy process, a type of macroautophagy, is the targeted removal of mitochondria. It is a type of autophagy exclusive to mitochondria, as the process removes defective mitochondria one by one. Mitophagy serves as an additional level of quality control by using autophagy to remove superfluous mitochondria or mitochondria that are irreparably damaged.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!