# Characterizing Novel Regulations of Dendritic Tiling in C. elegans

> **NIH NIH F31** · ALBERT EINSTEIN COLLEGE OF MEDICINE · 2021 · $15,173

## Abstract

PROJECT SUMMARY
Neurons rely on dendrites for the acquisition of sensory and synaptic input from their particular receptive fields.
Findings of aberrant dendritic morphology in disorders such as autism spectrum disorder (ASD) and
schizophrenia highlight the importance of understanding how complex dendritic arbors are developed and
maintained. During development, one of the goals of dendritic outgrowth is non-redundant coverage of a
receptive field, which requires the avoidance of other dendrites both from the same neuron (self-avoidance) and
from others (tiling). Tiling is evident in the organization of sensory neurites, such as those of C. elegans
mechanosensory neurons, drosophila dendritic arborization (da) neurons, and vertebrate retinal ganglion cells.
While tiling is a conserved property of many nervous systems, the molecular mechanisms by which it is
established remain unclear. The goal of this project is to uncover the genetic and molecular mechanisms of
dendritic tiling using the multi-dendritic FLP and PVD mechanosensory neurons of C. elegans as a model. The
dendritic arbor of FLP covers the head of the worm while the arbor of PVD covers the body. While previous
studies have identified both cell autonomous and cell non-autonomous cues for self-avoidance in outgrowing
PVD dendrites, the mechanisms by which FLP and PVD establish distinct non-overlapping receptive fields
remains unknown. From a pilot forward genetic screen, I have identified unc-33 as a gene required for the
specification of FLP and PVD receptive field size. Unc-33 is a member of the Collapsin Response Mediator
Protein (CRMP) family and is known to regulate axon development through the organization of microtubules.
While the role of unc-33 in axon outgrowth is well-characterized, its role in dendritic tiling is unclear. In the first
Aim of this project, I will use time-lapse imaging and cell ablation experiments to characterize the normal
development of tiling between FLP and PVD neurons. In the second Aim of this project, I will use genetic and
molecular techniques to determine the mechanism of action of unc-33 in regulating FLP and PVD tiling. In the
third Aim of this project, I will use a combined candidate and forward genetic approach to identify novel regulators
of tiling between FLP and PVD neurons. The results from this project will establish FLP and PVD as a new model
for the study of dendritic tiling and identify novel pathways regulating this process. Understanding the basic
mechanisms for the development for dendritic morphology will provide a foundation from which to understand
how these mechanisms are altered in neurodevelopmental disorders.

## Key facts

- **NIH application ID:** 10204136
- **Project number:** 5F31NS111939-03
- **Recipient organization:** ALBERT EINSTEIN COLLEGE OF MEDICINE
- **Principal Investigator:** Meera P Trivedi
- **Activity code:** F31 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2021
- **Award amount:** $15,173
- **Award type:** 5
- **Project period:** 2019-07-01 → 2021-10-30

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10204136

## Citation

> US National Institutes of Health, RePORTER application 10204136, Characterizing Novel Regulations of Dendritic Tiling in C. elegans (5F31NS111939-03). Retrieved via AI Analytics 2026-05-23 from https://api.ai-analytics.org/grant/nih/10204136. Licensed CC0.

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