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.
- Gabaldón C, Legüe M, Palominos MF, Verdugo L, Gutzwiller F, Calixto A. 2020. Intergenerational pathogen-induced diapause in Caenorhabditis elegans is modulated by mir-243. mBio 11:e01950-20. https://doi.org/10.1128/mBio.01950-20.
- Palominos, M. and Calixto, A. (2020). Quantification of Bacteria Residing in Caenorhabditis elegans Intestine. Bio-protocol 10(9): e3605. DOI: 10.21769/BioProtoc.3605.
- Arles Urrutia, Victor A. Garcia, Andres Fuentes, Mauricio Caneo, Marcela Legüe, Sebastián Urquiza, Juan Ugalde, Paula Burdisso, Andrea Calixto. Bacterially produced metabolites protect neurons from degeneration Plos Biology, 2020. 18(3): e3000638. https://doi.org/10.1371/journal.pbio.3000638
- Mauricio Caneo, Victoria Julian, Alexandra B. Byrne, Mark J. Alkema, and Andrea Calixto. Diapause induces functional axonal regeneration after necrotic insult in C. elegans. PLoS Genet. 2019 Jan 14;15(1):e1007863. doi: 10.1371/journal.pgen.1007863. eCollection 2019 Jan.
- Francisco Chavez and Andrea Calixto. Use of C. elegans diapause to study transgenerational responses to pathogen infection Methods Mol Biol. 2019;1918:191-197. doi: 10.1007/978-1-4939-9000-9_16.
- Legue M and Calixto A. RNA language in Caenorhabditis elegans and bacteria interspecies communication and memory. Current Opinion in Systems Biology. Volume 13, February 2019, doi.org/10.1016/j.coisb.2018.08.005 .
- Palominos MF, Verdugo L, Gabaldon C, Pollak B, Ortíz-Severín J, Varas M, Chávez FP, and Calixto A. Transgenerational Diapause as an Avoidance Strategy against Bacterial Pathogens in Caenorhabditis elegans. mBio 8:5 september/ october; doi:10.1128/mBio.01234-17 (2017).
- Calixto A. Life without food and the implications for neurodegeneration. Advances in Genetics, Volume 92. http://dx.doi.org/10.1016/bs.adgen.2015.09.004. (2015)
- Kelley M, Yochem J, Krieg M, Calixto A, Heiman MG, Kuzmanov A, Meli V, Chalfie M, Goodman MB, Shaham S, Frand A, Fay DS. 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 (2015)
- Calixto A, Jara JS, Court FA. Diapause Formation and Downregulation of Insulin-Like Signaling via DAF16/FOXO Delays Axonal Degeneration and Neuronal Loss. PLoS Genet 8(12): e1003141. doi:10.1371/journal.pgen.1003141 (2012)
- Calixto A, Chelur D, Topalidou I, Xiaoyin Chen and Chalfie M. Enhanced neuronal RNAi in C. elegans using SID-1. Nature Methods 7, 554-559 (2010).
- Calixto A, Ma C and Chalfie M. Conditional gene expression and RNAi using MEC-8- dependent splicing in C.elegans. Nature Methods 7, 407–411 (2010).