Talk:Fertilization

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2010

Mechanisms of sperm-egg interactions: between sugars and broken bonds

Sci Signal. 2010 Oct 5;3(142):pe35.

Visconti PE, Florman HM.

Department of Veterinary and Animal Sciences, University of Massachusetts, Amherst, MA 01003, USA. pvisconti@vasci.umass.edu Abstract A model of the early events of mammalian fertilization has emerged during the past 30 years. However, studies during the past decade have used newly available mouse models to readdress these processes. Here, we will consider these new data in light of the existing model and point to areas of reconciliation and of controversy.

PMID: 20923932 http://www.ncbi.nlm.nih.gov/pubmed/20923932

http://stke.sciencemag.org/cgi/content/full/sigtrans;3/142/pe35

Paper suggests the following 3 models for Mouse Models of sperm binding to the ZP.

1. The glycan model - Sperm bind by interacting selectively with O-glycans conjugated to ZP3 at Ser332, Ser334, or both residues. Sperm fail to bind after fertilization because of the enzymatic modification of the adhesion glycan by an egg glycosidase.

2. The supermolecular structure model - The sperm binding site is not specified (shown as including elements of ZP2 and ZP3). Access to this binding site is regulated by proteolytic cleavage of ZP2, such that after fertilization sperm are restricted from this site and cannot bind to the ZP.

3. A hybrid model - Sperm bind to an O-glycan that is conjugated to ZP3 at a site other than Ser332 or Ser334. Sperm access to this glycan is regulated by the proteolytic cleavage state of ZP2.

The role and regulation of sperm gelsolin prior to fertilization

J Biol Chem. 2010 Oct 11.

Finkelstein M, Etkovitz N, Breitbart H.

Bar-Ilan University, Israel. Abstract In order to acquire fertilization competence, spermatozoa should undergo several biochemical changes in the female reproductive tract, known as capacitation. The capacitated spermatozoon can interact with the egg zona-pellucida resulting in the occurrence of the acrosome reaction, a process which allowed its penetration into the egg and fertilize it. Sperm capacitation requires actin polymerization, while F-actin must disperse prior to the acrosome reaction. Here we suggest that the actin severing protein, gelsolin, is inactive during capacitation and is activated prior to the acrosome reaction. The release of bound gelsolin from phosphatidylinositol 4,5-bisphosphate (PIP(2)) by PBP10, a peptide containing the PIP2-binding domain of gelsolin, or by activation of PLC which hydrolyses PIP(2), caused rapid Ca(2+)-dependent F-actin depolymerization as well as enhanced acrosome reaction. Using immunoprecipitation assays, we showed that the tyrosine kinase SRC and gelsolin coimmunoprecipitate, and activating SRC by adding 8Br-cAMP enhanced the amount of gelsolin in this precipitate. Moreover, 8Br-cAMP enhanced tyrosine phosphorylation of gelsolin and its binding to PIP(2(4,5)), both of which inactivated gelsolin, allowing actin polymerization during capacitation. This actin polymerization was blocked by inhibiting the Src-family-kinases, suggesting that gelsolin is activated under these conditions. These results are further supported by our finding that PBP10 was unable to cause complete F-actin breakdown in the presence of 8Br-cAMP or vanadate. In conclusion, inactivation of gelsolin during capacitation occurs by its binding to PIP(2) and tyrosine phosphorylation by SRC. The release of gelsolin from PIP(2) together with its dephosphorylation enables gelsolin activation, resulting in the acrosome reaction.

PMID: 20937821 http://www.ncbi.nlm.nih.gov/pubmed/20937821


Sperm head binding to epithelium of the oviduct isthmus is not an essential preliminary to mammalian fertilization - review

Zygote. 2010 Jul 21:1-5.

Hunter RH.

Institute for Reproductive Medicine, Hannover Veterinary University, Bünteweg 15, D-30559 Hannover, Germany. Abstract SummaryIn endeavouring to understand the nature of sperm-oviduct interactions in mammals, attention was focused on experimental models in which fertilization can occur without a preliminary phase of sperm head binding to the isthmus epithelium. The ovarian endocrine milieu imposed on the oviduct tissues plays an important role in the binding phenomenon, although less so after the time of ovulation. Nonetheless, a sperm suspension introduced into the peritoneal cavity or surgical insemination directly into the oviduct ampulla before ovulation can result in fertilization, as can a surgical model in which the isthmus has been resected and the remaining portions of the duct reanastomosed. Mating or artificial insemination after ovulation in pigs permits rapid sperm transport to the site of fertilization, and the frequency of polyspermic penetration increases with the post-ovulatory age of eggs.Strategies underlying sperm binding were considered, especially in terms of preovulatory sperm storage and suppression of full membranous maturation. These, in turn, raised the problem of how sperm binding in vitro to oviduct cells from prepuberal animals or to cells harvested during the luteal phase of the estrous cycle, or to cells from the ampulla or even the tracheal epithelium, can act to regulate sperm storage and maturation with precision. In an evolutionary perspective, preovulatory binding of diverse populations of cells to the endosalpinx may have developed as a form of fine tuning to assist in sperm selection, to synchronize completion of capacitation with the events of ovulation, and to promote monospermic fertilization by a controlled release of competent gametes.

PMID: 20663263 http://www.ncbi.nlm.nih.gov/pubmed/20663263

2009

Etiology of sperm immunity in women

Fertil Steril. 2009 Feb;91(2):639-43. Epub 2008 Feb 20.

Clarke GN.

Andrology Unit, Royal Women's Hospital, Melbourne, Victoria, Australia. gary.clarke@rch.org.au

Abstract Sperm immunity in females can reduce the likelihood of natural conception, and sperm antibodies from female sera have been shown to inhibit IVF in humans and in several animal models. The etiology of sperm immunity in human females is unknown, but several possible mechanisms have been proposed, including cross-reactivity with microbial antigens and interferon gamma-mediated potentiation of the antisperm immune response in women whose male partners have sperm autoantibodies in their semen. This article reviews these ideas and postulates a novel hypothesis based on the potential for the generation of anti-idiotype antibodies in women whose partners have sperm antibodies in their semen.

PMID: 18281044

http://www.ncbi.nlm.nih.gov/pubmed/18281044


Egg coat proteins activate calcium entry into mouse sperm via CATSPER channels

Xia J, Ren D. Biol Reprod. 2009 Jun;80(6):1092-8. Epub 2009 Feb 11. PMID: 19211808

2008

IJDB

Vol. 52 Nos. 5/6 (2008) Fertilization

http://www.ijdb.ehu.es/web/contents.php?vol=52&issue=5-6


Sperm binding to the zona pellucida is not sufficient to induce acrosome exocytosis.

Baibakov B, Gauthier L, Talbot P, Rankin TL, Dean J. Development. 2007 Mar;134(5):933-43. PMID: 17293534

ZP2 and ZP3 traffic independently within oocytes prior to assembly into the extracellular zona pellucida

Hoodbhoy T, Avilés M, Baibakov B, Epifano O, Jiménez-Movilla M, Gauthier L, Dean J. Mol Cell Biol. 2006 Nov;26(21):7991-8. PMID: 17047254


inactive X chromosome

Cell cycle-dependent localization of macroH2A in chromatin of the inactive X chromosome. Chadwick BP, Willard HF. J Cell Biol. 2002 Jun 24;157(7):1113-23. Epub 2002 Jun 24. PMID: 12082075 \ JCB


Histone modifications and nuclear architecture: a review.

Bártová E, Krejcí J, Harnicarová A, Galiová G, Kozubek S.

J Histochem Cytochem. 2008 Aug;56(8):711-21. Epub 2008 May 12. Review.PMID: 18474937

2007

Establishment of the mammalian membrane block to polyspermy: evidence for calcium-dependent and -independent regulation

Reproduction. 2007 Feb;133(2):383-93.

Gardner AJ, Williams CJ, Evans JP.

Division of Reproductive Biology, Department of Biochemistry and Molecular Biology, Bloomberg School of Public Health, Johns Hopkins University, Baltimore, Room W3606, 615 N. Wolfe St., Maryland, USA. Abstract One crucial result of egg activation is the establishment of blocks on the zona pellucida and the egg plasma membrane to prevent fertilization by additional sperm. The mechanism(s) by which a mammalian egg regulates the establishment of the membrane block to polyspermy is largely unknown. Since Ca(2+) signaling regulates several egg activation events, this study investigates how sperm-induced Ca(2+) transients affect the membrane block to polyspermy, building on our previous work (Biology of Reproduction 67:1342). We demonstrate that mouse eggs that experience only one sperm-induced Ca(2+) transient establish a membrane block that is less effective, than in eggs that experience normal sperm-induced Ca(2+) transients but that is more effective than in eggs with completely suppressed [Ca(2+)](cyt) increases. Sperm-induced increases in [Ca(2+)](cyt) regulate the timing of membrane block establishment, as this block is established more slowly in eggs that experience one or no sperm-induced Ca(2+) transients. Finally, our studies produce the intriguing discovery that there is also a Ca(2+)-independent event that is associated with fertilization in the pathway leading to membrane block establishment. Taken together, these data indicate that Ca(2+) plays a role in facilitating membrane block establishment by regulating the timing with which this change in egg membrane function occurs, and also that the membrane block differs from other post-fertilization egg activation responses as Ca(2+) is not the only stimulus. The membrane block to polyspermy in mammalian eggs is likely to be the culmination of multiple post-fertilization events that together modify the egg membrane's receptivity to sperm.

PMID: 17307906