Andrea Calixto

Assistant Professor, Centro de Genomica y Bioinformática
Facultad de Ciencias, Universidad Mayor (2012-present)
Centro Interdisciplinario de Neurociencia de Valparaíso (CINV)
Ph.D. Columbia University (2009)

Curriculum Vitae

Contact information:
Telefono: 56-2-23289224

Research Overview

We aim at understanding how dietary inputs modify cellular phenotype and behavior. To this end, we use the bacterivore nematode Caenorhabditis elegans and its different bacterial diets. Both nematode and bacteria are genetically tractable which allows us to determine specific molecules from the microbe causing a measurable phenotype or behavioral change in the worm and the underlying changes in gene expression. We analyze the transcriptome of bacteria and worm under specific conditions to identify candidate molecules, followed by functional in vivo validation.

Neuronal protection. We use a model of genetically triggered neuronal degeneration of the gentle touch circuit in C. elegans, to study bacterial metabolites that delay and repair dying neurons. Additionally, we analyze the changes in the worm´s transcriptome, to identify genes that change in response to bacterial diets that promote neuronal protection.

Long-term strategies of survival under pathogenesis. We study the molecular triggers of transgenerational transmission of information that ensures long-term survival of populations of animals. Specifically, we hypothesize that in the pair pathogenic bacteria-worm, bacteria communicates with the animal in the form of small RNAs, which are processed by the RNAi machinery and give rise to an endogenous response that triggers the behavioral response.


Calixto A. (2015) Life without Food and the Implications for Neurodegeneration. Adv Genet. 2015;92:53-74. doi: 10.1016/bs.adgen.2015.09.004. Review.

Kelley M, Yochem J, Krieg M, Calixto A, Heiman MG, Kuzmanov A, Meli V, Chalfie M, Goodman MB, Shaham S, Frand A, Fay DS. (2015) FBN-1, a fibrillin-related protein, is required for resistance of the epidermis to mechanical deformation during C. elegans embryogenesis. eLife Mar 23;4.doi: 10.7554/eLife.06565. 

Calixto A, Jara JS, Court FA. (2012) Diapause Formation and Downregulation of Insulin-Like Signaling via DAF-16/FOXO Delays Axonal Degeneration and Neuronal Loss. PLoS Genet 8(12): e1003141. doi:10.1371/journal.pgen.1003141 . 

Calixto A, Chelur D, Topalidou I, Xiaoyin Chen and Chalfie M. (2010) Enhanced neuronal RNAi in C. elegans using SID-1. Nature Methods 7, 554-559 . 

Calixto A, Ma C and Chalfie M. (2010) Conditional gene expression and RNAi using MEC-8- dependent splicing in C.elegans. Nature Methods 7, 407–411 . 

Huber TB, Schermer B, Müller RU, Höhne M, Bartram M, Calixto A, Hagmann H, Reinhardt C, et al. (2006) Podocin and MEC-2 bind cholesterol to regulate the activity of associated ion channels. Proc. Natl. Acad. Sci. U S A. 103; 17079-86 .

Lehner B, Calixto A, Crombie C, Tischler J, Fortunato A, Chalfie M, Fraser AG. (2006) Loss of LIN-35, the Caenorhabditis elegans ortholog of the tumor suppressor p105Rb, results in enhanced RNA interference. Genome Biol.7:R4 . 

Lettre G, Kritikou EA, Jaeggi M, Calixto A, Fraser AG, Kamath RS, Ahringer J, Hengartner MO. (2004) Genome-wide RNAi identifies p53-dependent and -independent regulators of germ cell apoptosis in C. elegans. Cell Death Differ. 11:1198-203 .


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