# Elucidating the Mechanistic Basis for Phagotrophy in the Protozoan Trypanosoma cruzi (equipment supplement)

> **NIH NIH R01** · UNIVERSITY OF GEORGIA · 2023 · $200,000

## Abstract

Being able to efficiently extract nutrients from one’s environment is an essential activity for any heterotroph
ranging from predators to parasites. Among the free-living planktonic protozoans, the extremely diverse class
of phagotrophic predators have devised a variety of methods to capture and consume the sources of organic
carbon they need to grow and reproduce. One of the most widespread modes of mechanical predation
employed by these protozoa involves cilia or flagella supported filter feeding. Captured prey are ultimately
endocytosed via a cell spanning tubular invagination, originating at a pore in the plasma membrane, and
ending in budding vesicles targeted for lysosomal digestion. This pore (cytostome), and its emanating tubule
structure (cytopharynx), are collectively referred to here as the cytostome/cytopharynx complex (SPC).
Despite its ubiquitous presence, almost nothing is known about how the SPC is generated or functions at
the molecular level in any organism. It is worth noting that, collectively, the SPC containing protozoa play
critical roles in diverse activities ranging from the global microbial food web to human parasitism. Intriguingly,
the genetically tractable flagellate, Trypanosoma cruzi, has retained this ancestral mode of endocytosis and,
much like it’s free-living bacterivorous relatives (e.g. Bodo saltans), actively endocytoses its host’s material
sustenance via the SPC as well. How protozoans capture food at their surface, signal internally to initiate
endocytosis and ultimately traffic this material down the SPC to the lysosome for digestion remains a
mystery and is at the core of the questions we seek to answer in this proposal. We have found that SPC-
mediated endocytosis is dispensable for T. cruzi when grown in vitro, and as a result, we are uniquely
positioned to be able to conduct extensive knockout (KO) and complementation studies to functionally dissect
multiple dimensions of SPC function without impacting cell viability for the first time. As a continuation of our
prior published work, this proposal seeks to generate a holistic understanding of how SPC mediated
endocytosis fundamentally functions. We will begin by dismantling the unified activity of endocytosis into its
constituent processes; cargo capture through surface receptors (Aim1), receptor signal transduction and
activation of endocytic machinery (Aim2) and finally active transport of phagocytosed cargo along the SPC for
digestion (Aim3). Each of these aims will address important basic aspects of protozoan biology that continue to
remain poorly understood. As studies currently underway have highlighted, the use of standard confocal live
microscopy is too slow and toxic to study this highly dynamic and rapid process. As a result, this proposal
requests funding to support the acquisition of a spinning disk confocal microscope that will be capable of
imaging extremely fast protozoan endocytic activities across long periods of time without the concer...

## Key facts

- **NIH application ID:** 10799091
- **Project number:** 3R01GM144545-02S1
- **Recipient organization:** UNIVERSITY OF GEORGIA
- **Principal Investigator:** RONALD DREW ETHERIDGE
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2023
- **Award amount:** $200,000
- **Award type:** 3
- **Project period:** 2022-06-01 → 2026-04-30

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10799091

## Citation

> US National Institutes of Health, RePORTER application 10799091, Elucidating the Mechanistic Basis for Phagotrophy in the Protozoan Trypanosoma cruzi (equipment supplement) (3R01GM144545-02S1). Retrieved via AI Analytics 2026-05-24 from https://api.ai-analytics.org/grant/nih/10799091. Licensed CC0.

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