Heat Stress and the Bull Sperm Transcriptome: Molecular Mechanisms, Fertility, and Epigenetic Inheritance

Heat stress (HS) occurs when the body's physiological mechanisms for regulating body temperature are unable to cope with external conditions. Regarding male reproductive function, HS increases testicular temperature, leading to a reduction in sperm production and motility, and an increase in abnormal sperm, oxidative stress and DNA fragmentation. However, the molecular basis behind these induced HS changes has not been fully characterized. In bovine spermatozoa, post-transcriptional regulation of messenger RNA (mRNA) is activated during spermatogenesis, and mechanisms mediated by microRNAs (miRNAs) are involved in the control of gene expression throughout the germline differentiation. Furthermore, extracellular vesicles containing proteins, lipids, miRNAs, mRNAs, and long non-coding RNAs derived from seminal plasma and epididymis influence sperm motility, capacitation, and fertilization potential. Therefore, despite the fact that mature spermatozoa are in an inactive transcriptional state, these cells contain a complex population of RNAs playing a role in embryonic development, which can be exploited for research on and diagnosis of male infertility. This review aims to elucidate several aspects of bovine sperm physiology and molecular mechanisms. Particular attention is given to the cascade of functional, cellular, and molecular events triggered by elevated temperatures in mature spermatozoa to disclose strategies to mitigate HS effects and maintain bull fertility.