# Sliding vertex behaviors during epithelial morphogenesis and tissue elongation

> **NIH NIH R01** · UNIVERSITY OF DENVER (COLORADO SEMINARY) · 2020 · $294,910

## Abstract

Project Summary
Epithelial sheets sit at the boundary of the organism and its external environment. The
maintenance of these apical and basolateral domains is essential to the barrier function
of epithelia, and the loss of apical-basal polarity is associated with the metastasis of
many epithelial cancers. While epithelial sheets were once viewed as largely static
assemblies, it is now appreciated that these are dynamic structures that can undergo
significant reorganizing and renewal events. Indeed, cell neighbor exchange can be
harnessed by developmental processes to effect changes in tissue architecture, and cell
intercalation can drive epithelial tissue repair. In the Drosophila embryonic epithelium,
individual cells are able to either consolidate cell-cell contacts or direct neighbor
exchange movements through the contraction of vertical T1 interfaces and the
subsequent resolution of horizontal T3 interfaces. The dominant model in explaining
these behaviors has been one in which line tensions that stretch across interfaces direct
these changes. However, a number of observations have led us to question this
approach. Our central hypothesis is that cell vertices demonstrate radial coupling and
that the best explanation of intercalary behaviors will be through a description of the
radially-directed force events that lead to vertex movements and subsequent dependent
changes in interface lengths. Our data suggests that tricellular vertices slide along cell-
cell interfaces to harness radial forces, and would introduce a new area of research on
the molecular and biophysical contributions of cell vertices to embryogenesis. Pulsed
oscillations in cell area have been found to drive developmental processes in a number
of different systems and tissues, but the mechanisms that link these area oscillations to
productive tissue shaping events have been unclear. Because of this, we believe vertex
sliding through radial force coupling offers a new, fundamental mechanism that may
account for this conservation of oscillatory mechanics. We also will examine the
structure and oscillation of adhesion complexes that are located at cell vertices, as well
as the relationship between actomyosin forces and changes in vertex structure. We
believe the proposed studies will provide a fundamentally new vertex-based mechanism
that directs cell intercalation through junctional sliding driven by radial coupling.

## Key facts

- **NIH application ID:** 9998978
- **Project number:** 5R01GM127447-03
- **Recipient organization:** UNIVERSITY OF DENVER (COLORADO SEMINARY)
- **Principal Investigator:** James Todd Blankenship
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2020
- **Award amount:** $294,910
- **Award type:** 5
- **Project period:** 2018-09-20 → 2022-08-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/9998978

## Citation

> US National Institutes of Health, RePORTER application 9998978, Sliding vertex behaviors during epithelial morphogenesis and tissue elongation (5R01GM127447-03). Retrieved via AI Analytics 2026-05-23 from https://api.ai-analytics.org/grant/nih/9998978. Licensed CC0.

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