Pablo E. Visconti

Pablo E. Visconti


he, him, his


427W ISB

Office phone: 




Ph.D.: University of Buenos Aires, 1991
Postdoctoral Training: University of Pennsylvania

Rockefeller Foundation Postdoctoral Fellow, 1991-1995
Rayard Storey Award, 1999

Collaborating PIs
Ana Maria Salicioni, PhD
Maria Gracia Gervasi, PhD


ANIMLSCI 521 - Physiology of Reproduction

Research Interests

Signal Transduction Pathways During Sperm Capacitation

Mammalian sperm are not able to fertilize eggs immediately after ejaculation. They acquire fertilization capacity after residing in the female tract for a finite period of time. The physiological changes occurring in the female reproductive tract that render the sperm able to fertilize constitute the phenomenon of sperm capacitation.

Using the mouse as an experimental paradigm, we have demonstrated that conditions conducive to capacitation of cauda epididymal sperm promote the tyrosine phosphorylation of a subset of proteins of Mr 40,000 - 120,000. The increase in protein tyrosine phosphorylation is dependent on the presence of BSA, Ca2+ and NaHCO3 in the medium, and the concentrations of these compounds needed for protein tyrosine phosphorylation to occur are correlated with those required for capacitation.

Serum albumin, usually bovine serum albumin (BSA), is believed to function during capacitation in vitro as a sink for the removal of cholesterol from the sperm plasma membrane. We have demonstrated that cholesterol removal is also essential in the regulation of intracellular signaling that occurs during sperm capacitation.

The transmembrane movements of HCO3- and/or Ca2+ could be responsible for the regulation of sperm cAMP metabolism, since the mammalian sperm adenylyl cyclase is markedly stimulated by these ions. We have also demonstrated that the increase in protein tyrosine phosphorylation as well as capacitation were regulated by a cAMP-dependent pathway involving protein kinase A (PKA).

Simultaneously with our findings, Zeng et al. (Dev. Biol. 1995; 171:554-563) reported that capacitation is accompanied by hyperpolarization of the sperm plasma membrane. Although the molecular basis of capacitation is not well understood, recent work from many laboratories is beginning to lead to a unified hypothesis of how capacitation is controlled and this is summarized in the following model:

Transmembrane and intracellular signaling pathways hypothesized to play a role in regulating sperm capacitation. This model is based on the work from a number of different laboratories.


(-) indicates negative regulation;
(+) indicates positive regulation.
BSA: bovine serum albumin
Chol, cholesterol
5'AMP, 5' adenosine monophosphate; PTK, protein tyrosine kinase
PTyr-Ptase, phosphotyrosine phosphatase
PDE, cyclic nucleotide phosphodiesterase.


My long term goal is to understand how the sperm acquire fertilizing capacity at the molecular level. In particular, I am focusing in several basic questions that arise from the capacitation model in the figure such as:

  1. Which are the protein substrates for tyrosine phosphorylation and how are they involved in the capacitation process?
  2. Which are the tyrosine kinase/s and/or phosphotyrosine phosphatases responsible for the increase in protein tyrosine phosphorylation observed during capacitation?
  3. fig2How capacitation and the capacitation-associated hyperpolarization are regulated by components of the capacitation medium?
  4. How are changes in cAMP, protein tyrosine phosphorylation and hyperpolarization of the sperm plasma membrane integrated to regulate capacitation?
  5. Where in the sperm do the changes in cAMP, protein tyrosine phosphorylation and hyperpolarization occur during capacitation?
  6. How cholesterol removal affects signaling pathways during sperm capacitation?


Lab Personnel

Name Email Phone Office
Mohanty, Gayatri
Postdotoral Research Associate
gmohanty [at] 413-545-4050 ISB 465A
Nayyab, Saman
Graduate Student - MCB
snayyab [at] 413-545-4050 ISB 465A
Taghavi, Mahboubeh
Graduate Student - ABBS
mtaghavi [at] 413-545-4050 ISB 465A
Weber, W. David
Postdoctoral Research Associate
wweber [at] 413-545-4050 ISB 465A


Wang, F., Gervasi, M. Gracia, Bošković, A., Sun, F., Rinaldi, V. D., Yu, J., et al.. (2021). Deficient spermiogenesis in mice lacking . Elife, 10. presented at the 2021 02 23. doi:10.7554/eLife.63556
Gervasi, M. Gracia, & Visconti, P. E.. (2016). Chang's meaning of capacitation: A molecular perspective. Mol Reprod Dev. presented at the 2016 Jun 3.
Visconti, P. (2012). Sperm Bioenergetics in a Nutshell. Biology of reproduction. presented at the 2012 Aug 22.
Salicioni, A. M., Romano, F. B., & Visconti, P. E.. (2012). Testis-Specific Kinases in male Fertility and as Targets for Contraception. American Pharmaceutical Review, 15(5). presented at the 09/2012.
Sosnik, J., Buffone, M. G., & Visconti, P. E.. (2010). Analysis of CAPZA3 localization reveals temporally discrete events during the acrosome reaction. Journal of cellular physiology, 224(3), 575-80. presented at the 2010 Sep.
Visconti, P. E., & Florman, H. M.. (2010). Mechanisms of sperm-egg interactions: between sugars and broken bonds. Science signaling, 3(142), pe35. presented at the 2010.
Visconti, P. E. (2009). Understanding the molecular basis of sperm capacitation through kinase design. Proceedings of the National Academy of Sciences of the United States of America, 106(3), 667-8. presented at the 2009 Jan 20.
Arcelay, E., Salicioni, A. M., Wertheimer, E., & Visconti, P. E.. (2008). Identification of proteins undergoing tyrosine phosphorylation during mouse sperm capacitation. The International journal of developmental biology, 52(5-6), 463-72. presented at the 2008.
Salicioni, A. M., Platt, M. D., Wertheimer, E. V., Arcelay, E., Allaire, A., Sosnik, J., & Visconti, P. E.. (2007). Signalling pathways involved in sperm capacitation. Society of Reproduction and Fertility supplement, 65, 245-59. presented at the 2007.