Leeuwenhoek Institute/Reynevelt College, The Netherlands
B.Sc., Microbiology, 1993

Polytechnical College of Delft (HLO), The Netherlands
B.Sc., Biochemistry, 1996

University of Leiden, The Netherlands
M.Sc., Molecular Biology, 1999

University of Utrecht, Hubrecht Institute, The Netherlands
Ph.D. Biology, 2003

Brandeis University, MA
Postdoctoral Fellow, 2003-2009

Contact Information

University of Nevada, Reno
Department of Biology, Mailstop 314
Reno, NV 89557

email Dr. Alexander van der Linden
Office Phone:
Fax: 775-784-1302

Van der Linden Lab Homepage

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Research Interests

The availability and quality of food fluctuates over time in an animal’s environment. When food is scarce, an animal must undergo changes in its behavior, metabolism and development to promote survival. An animal must also regulate its feeding habits depending on nutritional status in order to maintain physiological homeostasis. Timing of feeding is also vital for an animal’s health; for instance, human shift workers with altered circadian rhythms and eating habits have an increased risk of developing metabolic disorders including obesity. We are interested in understanding how animals sense and adapt to environmental stimuli such as food, and how this information is translated into coordinated changes in behavior and development. To better understand these questions, we are using the nematode Caenorhabditis elegans as a genetic model system. Detailed knowledge of the relatively simple C. elegans nervous system combined with tractable genetic and genomic tools allow us to functionally dissect the neuronal circuits and molecular mechanisms underlying the regulation of food-induced responses.

C. elegans is able to modulate the expression of G-protein-coupled receptor (GPCR) genes in response to environmental signals such as constitutively produced pheromone and food. This provides a simple mechanism by which C. elegans can rapidly alter its sensory behaviors and development in response to changing conditions. We have identified several molecules that play key roles in the regulation of GPCR gene expression. In particular, we have found that the KIN-29/MEF-2-mediated pathway acts cell non-autonomously in the chemosensory system to regulate GPCR gene expression and food-induced responses such as body size and dauer entry. KIN-29 function is also responsible for foraging and quiescence behavior. Our current studies are directed to better understand the KIN-29 pathway by which food-derived signals are integrated to modulate behavior and development, and to define the neuronal circuits that regulate these food-induced responses. We are also investigating the yet unidentified circadian clock in C. elegans, and are exploring the interaction between circadian clocks, metabolism and feeding behaviors.

Selected Publications

Van der Linden, A.M., Wiener S., You Y., Kim K., Avery L., and Sengupta, P. (2008) The EGL-4 PKG acts with the KIN-29 SIK and PKA to regulate chemoreceptor gene expression and sensory behaviors in C. elegans. Genetics Nov; 180(3): 1475-91.

Van der Linden, A.M., Nolan, K.M., and Sengupta, P. (2007) KIN-29 SIK regulates chemoreceptor gene expression via an MEF2 transcription factor and a class II HDAC. EMBO J. 26(2): 358-70.

Bauer Huang S.L., Saheki Y., VanHoven M.K., Torayama I., Ishihara T., Katsura I., Van der Linden A., Sengupta P. and Bargmann C.I. (2007) Left-right olfactory asymmetry results from antagonistic functions of voltage-activated calcium channels and the Raw repeat protein OLRN-1 in C. elegans. Neural Develop. Nov 6: 2:24.

Fitzgerald K., Tertyshnikova S., Moore L., Bjerke L., Burley B., Cao J., Carroll P., Choy R., Doberstein S., Dubaquie Y., Franke Y., Kopczynski J., Korswagen H., Krystek S.R., Lodge N.J., Plasterk R., Starrett J., Stouch T., Thalody G., Wayne H., Van der Linden A., Zhang Y., Walker S.G., Cockett M., Wardwell-Swanson J., Ross-Macdonald P. and Kindt R.M. (2006) Chemical genetics reveals an RGS/G-protein role in the action of a compound. PLoS Genet. 2(4)

Van der Linden, A.M. and Plasterk, R.H.A. (2004) Shotgun cloning of transposon insertions in the genome of Caenorhabditis elegans. Comp Funct Genomics 5(3): 225-29.

Simmer, F.*, Moorman, C.*, Van der Linden, A.M.*, Kuijk, E., van den Berghe, P.V., Kamath, R., Fraser, A.G., Ahringer, J., and Plasterk, R.H.A. (2003). Genome-wide RNAi of C. elegans using the hypersensitive rrf-3 strain reveals novel gene functions. PLoS Biol. 1: 77-84. * authors contributed equally

Van der Linden, A.M., Moorman, C., Cuppen, E., Korswagen, H.C. and Plasterk, R.H.A. (2003) Hyperactivation of the G12-mediated signaling pathway in Caenorhabditis elegans induces a developmental growth arrest via protein kinase C. Current Biology 13: 516-521.

Cuppen E., Van der Linden A.M., Jansen G. and Plasterk R.H. (2003) Proteins interacting with Caenorhabditis elegans Ga subunits. Comp Funct Genomics 4(5): 479-91.

Van der Linden, A.M., Simmer, F., Cuppen, E., and Plasterk, R.H.A. (2001) The G-protein ß-subunit GPB-2 in Caenorhabditis elegans Regulates the Goa-Gqa Signaling network through interactions with the regulator of G-protein signaling proteins EGL-10 and EAT-16. Genetics 158: 221-235.

Korswagen, H.C., Van der Linden, A.M. and Plasterk, R.H.A. (1998) G-protein hyperactivation of the Caenorhabditis elegans adenylyl cyclase SGS-1 induces neuronal degeneration. EMBO J. 17: 5059-5065