Claire Richardson

Position title: Assistant Professor


Neurobiology, cell biology, aging and stress, genetics, C. elegans

425 Henry Mall, room 4106
Ph.D., MIT (2012), Postdoctoral Research: Stanford University.
Research Interests
Molecular and cellular neurobiology in health and in aging.

Lab Website:

Research Description:

Neurons live as long as the animal in which they reside. For humans, this means that our neurons can live for 100 years or more. Over the decades of our lives, we show signs of aging – our skin becomes wrinkled, our hair turns gray. Our neurons likewise show signs of aging, features of which include decreased morphological abnormalities, synapse loss, glucose hypometabolism, and mitochondrial dysfunction. This is problematic for health: first, aging is often accompanied by cognitive decline, and second, aging is by far the primary risk factor for dementia and neurodegenerative disease. The Richardson Lab use the nematode Caenorhabditis elegans to ask, what causes neuronal aging, and can it be prevented?

C. elegans has evolved the remarkable ability to de-couple the symptoms of aging from chronological age. Normally, C. elegans age and die in two weeks. However, in the alternate organismal state called “dauer,” animals pause all growth and development programs and survive for months. Neurons remain functional, but features of neuronal aging are likewise stalled. We exploit this phenotypic plasticity to investigate how neuron aging can be stalled.

We are particularly interested in the interplay between neuronal aging and endosomes. Aberrant endosome morphology and function is associated with neurodegenerative diseases. We hypothesize that there is a conserved role for the endocytic pathway in promoting the pathologies associated with neuronal aging.

Synaptic vesicles are a highly specialized type of endosome used for the rapid communication of firing activity between connected neurons in a circuit. We are interested in the regulation of synaptic vesicle homeostasis in development versus adulthood, and what causes synaptic vesicle homeostasis to decline in aging.

Representative Publications:

Liu J, Kim YS, Richardson CE, Tom A, Ramakrishnan C, Birey F, Katsumata T, Chen S, Wang C, Wang X, Joubert LM, Jiang Y, Wang H, Fenno LE, Tok JB, Pașca SP, Shen K, Bao Z, Deisseroth K. Genetically targeted chemical assembly of functional materials in living cells, tissues, and animals. Science. 2020 Mar 20;367(6484):1372-1376. doi: 10.1126/science.aay4866. PubMed PMID: 32193327; PubMed Central PMCID: PMC7527276.

Richardson CE, Yee C, Shen K. A hormone receptor pathway cell-autonomously delays neuron morphological aging by suppressing endocytosis. PLoS Biol. 2019 Oct;17(10):e3000452. doi: 10.1371/journal.pbio.3000452. eCollection 2019 Oct. PubMed PMID: 31589601; PubMed Central PMCID: PMC6797217.

Richardson CE, Shen K. Neurite Development and Repair in Worms and Flies. Annu Rev Neurosci. 2019 Jul 8;42:209-226. doi: 10.1146/annurev-neuro-070918-050208. Epub 2019 Mar 18. Review. PubMed PMID: 30883262.

Richardson CE, Spilker KA, Cueva JG, Perrino J, Goodman MB, Shen K. PTRN-1, a microtubule minus end-binding CAMSAP homolog, promotes microtubule function in Caenorhabditis elegans neurons. Elife. 2014 Feb 25;3:e01498. doi: 10.7554/eLife.01498. PubMed PMID: 24569477; PubMed Central PMCID: PMC3932522.

Richardson CE, Kooistra T, Kim DH. An essential role for XBP-1 in host protection against immune activation in C. elegans. Nature. 2010 Feb 25;463(7284):1092-5. doi: 10.1038/nature08762. PubMed PMID: 20182512; PubMed Central PMCID: PMC2834299.