“Centro Interdisciplinario de Neurociencia de Valparaíso”.
Research Area: Cytoskeleton dynamics and vesicle trafficking in neuroendocrine and muscle cells.
Neurosecretion Laboratory, Professor Ana María Cárdenas Díaz
Ph.D. in Sciences (Mention in Neuroscience) Universidad de Valparaíso, Chile (2013).
Graduate in Biochemist, Universidad Católica de Valparaíso, Chile (2007)
E-mail: arlek.gonzalez at cinv.cl, arlek.gonzjam at gmail.com
Fax: (56)-(32)-250 1111
Address: Centro Interdisciplinario de Neurociencia de Valparaíso.
Facultad de Ciencias, Universidad de Valparaíso.
Gran Bretaña 1111. Playa Ancha. Valparaíso. Chile.
In the last years I have been interested in understanding the function and the regulatory role of the GTPase dynamin on several cellular processes. During my Doctoral thesis project I demonstrated that the ubiquitously expressed isoform dynamin-2 is pivotal for a proper actin cytoskeleton dynamics in neuroendocrine chromaffin cells. This regulation seems to be critical to control the characteristics of the secretory processes since both, dynamin-2 and cortical actin, participate adjusting the kinetics and the amount of transmitters released during secretion. These findings were published the last year in Plos One (González-Jamett AM, Momboisse F, Guerra MJ, Ory S, Báez-Matus X, et al. (2013) Dynamin-2 regulates fusion pore expansion and quantal release through a mechanism that involves actin dynamics in neuroendocrine chromaffin cells. PLoS One 8: e70638).
Currently, I am focused on understanding how different mutations in the gene encoding dynamin-2, which associate to a congenital neuromuscular disorder called Centro Nuclear Miopathy (CNM), impact on dynamin-2 dependent processes leading to CNM. By using Confocal and Total Internal Reflection Fluorescence (TIRF) microscopy I have observed that two mutations located into the middle domain of dynamin-2 (R465W and R369W) suppress the new formation of actin filaments and modify the actin organization pattern in a human skeletal muscle cell line (RCMH). These effects are similar to those observed by pharmacological inhibition of dynamin. Interestingly dynamin´s inhibition also disrupts the trafficking of the glucose transporter GLUT-4 in RCMH cells, a mechanism that reportedly depends on actin dynamics, suggesting that this may be an affected pathway in MCN.
- Alvaro O. Ardiles, Arlek M González-Jamett, Jaime Maripillan, David Naranjo, Pablo Caviedes, Ana María Cárdenas. (2007) Calcium Channel Subtypes Differentially Regulate Fusion Pore Stability And Expansion. Journal of Neurochemistry; 4, 1574-1581.
- Gonzalez-Jamett AM, Báez-Matus X, Hevia MA, Guerra MJ, Olivares MJ, Martínez AD, Neely A, Cárdenas AM (2010) The association of dynamin with synaptophysin regulates quantal size and duration of exocytotic events in chromaffin cells. J. Neurosci. 30: 10683 – 10691.
- González-Jamett AM, Momboisse F, Guerra MJ, Ory S,Baez-Matus X, Barraza N, Calco V, Houy S, Couve E, Neely A, Martínez A, Gasman S, Cárdenas AM (2013) Dynamin-2 regulates fusion pore expansion and quantal release through a mechanism that involves actin dynamics in neuroendocrine chromaffin cells. PLoS One 8: e70638. PDF
- González-Jamett AM, Momboisse F, Haro-Acuña V, Bevilacqua JA, Caviedes P, Cardenas AM (2013) Dynamin-2 function and dysfunction along the secretory pathway. Front. Endocrinol. (Lausanne), 4: 126 (DOI: 10.3389/fendo.2013.00126). PDF
- González-Jamett AM, Haro-Acuña V, Momboisse F, Caviedes P, Bevilacqua JA, Cárdenas AM (2014) Dynamin-2 in nervous system disorders. J. Neurochem 128(2):210-23.
- Olivares MJ, González-Jamett AM, Guerra MJ, Baez-Matus X, Haro-Acuña V, Martínez-Quiles N, Cárdenas AM (2014) Src kinases regulate de novo actin polymerization during exocytosis in neuroendocrine chromaffin cells (Plos One, submitted).