Publications by authors named "Dalen Zuidema"

The degradation of sperm-borne mitochondria after fertilization is a conserved event. This process known as post-fertilization sperm mitophagy, ensures exclusively maternal inheritance of the mitochondria-harbored mitochondrial DNA genome. This mitochondrial degradation is in part carried out by the ubiquitin-proteasome system.

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Artificial insemination of livestock has been a staple technology for producers worldwide for over sixty years. This reproductive technology has allowed for the rapid improvement of livestock genetics, most notably in dairy cattle and pigs. This field has experienced continuous improvements over the last six decades.

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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.

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The ubiquitin-proteasome system plays diverse regulatory and homeostatic roles in mammalian reproduction. Ubiquitin ligases are the substrate-specific mediators of ubiquitin-binding to its substrate proteins. The NEDD4-like ubiquitin ligase 2 (aliases NEDL2, HECW2) is a HECT-type ubiquitin ligase that contains one N-terminal HECW ubiquitin ligase domain, one C-terminal HECT ubiquitin ligase domain, one C2 domain, and two WW protein-protein interaction modules.

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Mammalian fertilization remains a poorly understood event with the vast majority of studies done in the mouse model. The purpose of this review is to revise the current knowledge about semen deposition, sperm transport, sperm capacitation, gamete interactions and early embryonic development with a focus on the porcine model as a relevant, alternative model organism to humans. The review provides a thorough overview of post-ejaculation events inside the sow's reproductive tract including comparisons with humans and implications for human fertilization and assisted reproductive therapy (ART).

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Maternal mitochondrial inheritance is a fundamental paradigm within reproductive biology, yet the molecular mechanisms which underlie this process remain poorly understood. The ubiquitin proteasome system (UPS) and branches of the autophagic pathway have been implicated in taking part in the active degradation of sperm mitochondria post-fertilization. Despite this knowledge, there remains much unknown about this process, including the cofactors and substrates involved, as well as the implications of what occurs when these systems of degradation fail.

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Critical to fertilization success, sperm capacitation within the female oviductal sperm reservoir endows mammalian spermatozoa with hyperactivated motility and capacity to fertilize. An elaborate cascade of signaling events during capacitation guides the redistribution of sperm plasma membrane seminolipid and cholesterol, Ca-influx and increases tyrosine phosphorylation to promote hyperactivated motility. Such events result in the remodeling of the sperm acrosome, increased fluidity and fusability of the plasma membrane, shedding of surface-adsorbed seminal plasma proteins that glue sperm heads to the oviductal epithelium and ultimately the release of hyperactivated spermatozoa from the oviductal sperm reservoir.

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