Plcz1 Deficiency Decreased Fertility in Male Mice Which Is Associated with Sperm Quality Decline and Abnormal Cytoskeleton in Epididymis.
Tao WangBinbin CaoYao CaiSi ChenBaozhu WangYan YuanQuan ZhangPublished in: International journal of molecular sciences (2022)
Phospholipase C zeta1 (Plcz1) was known to be a physiological factor in sperm that activates oocytes to complete meiosis by triggering Ca 2+ oscillations after fertilisation. However, the role of male Plcz1 in spermatogenesis and early embryo development in progeny has been controversial. Plcz1 knockout ( Plcz1 -/- ) mouse model ( Plcz1 m3 and Plcz1 m5 ) was generated by using the CRISPR-Cas9 system. The fertility of Plcz1 -/- mice was evaluated by analysing the number of offsprings, sperm quality, pathological changes in the testis and epididymis. RNA-seq and RT-PCR were performed to screen differentially expressed genes and signalling pathways related to fertility in Plcz1 -/- mice. Further mechanism was explored by using Plcz1 -/- cells. Plcz1 knockout led to hypofertility in male mice. In particular, a significant time delay in development and polyspermy was found in eggs fertilized by both Plcz1 m3 and Plcz1 m5 sperm. Interestingly, a decline in sperm quality combined with pathological changes in epididymis was found in Plcz1 m3 mice but not in Plcz1 m5 mice. Notably, abnormal cytoskeleton appears in epididymis of Plcz1 m3 mice and Plcz1 -/- cells. Cytoskeleton damage of epididymis is involved in fertility decline of males upon Plcz1 deficiency in this model.
Keyphrases
- crispr cas
- rna seq
- high fat diet induced
- induced apoptosis
- single cell
- gene expression
- genome editing
- oxidative stress
- high throughput
- signaling pathway
- skeletal muscle
- genome wide
- wild type
- working memory
- quality improvement
- endoplasmic reticulum stress
- cell cycle arrest
- young adults
- drug induced
- childhood cancer
- protein kinase