# Investigations of the role of host controlled peptidoglycan recycling in the regulation of the pea aphid-Buchnera symbiosis

> **NIH NIH F32** · UNIVERSITY OF TEXAS AT AUSTIN · 2020 · $17,327

## Abstract

Project Summary
 Animals live in close association with bacteria, including both beneficial symbionts and harmful
pathogens. Understanding the nuances that enable hosts to respond differently to pathogenic versus beneficial
interactions could enable therapies that specifically target pathogens. A fundamental interface between
bacterial and animal cells is the bacterial cell wall. In particular, cell wall peptidoglycan (PG) is known to be a
key molecule in the infection process, both for pathogens such as Bordetella pertussis and Neisseria
gonorrhoeae and also for symbionts such as Vibrio fischeri. In the model symbiosis of the pea aphid,
Acyrthosiphon pisum, with its bacterial symbiont, Buchnera aphidicola, key enzymes in the pathway for PG
recycling are encoded in the host genome and are known to be specifically expressed in the cells that harbor
the symbiotic bacteria, and similar observations have been made in other eukaryotic systems. The focus of this
proposal is to test the novel hypothesis that host control of PG recycling is a key mechanism for host regulation
of symbiont populations. We will test this hypothesis using novel biochemical and genetic approaches within
the pea aphid system. Specifically, we hypothesize that variation in Buchnera abundance between aphids can
be explained by differences in the level of host-derived PG gene expression, that the host employs proteins
that alter the Buchnera cell wall, and that host control over Buchnera PG recycling establishes stability of
Buchnera population sizes. Testing this hypothesis will shed light on how animals domesticate pathogenic
bacteria and convert them into symbionts, and, more broadly, will expand our fundamental understanding of
microbial interactions with animals, including humans.
 To define the role of PG recycling in the regulation of symbiosis, we will: 1) investigate whether PG-
related host genes play a role in determining Buchnera population size, 2) determine how host PG-related
genes interact functionally with the Buchnera cell wall, and 3) demonstrate the relationship between host PG
genes and Buchnera regulation in vivo. To test this, we will quantify the differences in PG gene expression
levels between aphid genotypes with high versus low Buchnera abundance, characterize how host gene
products affect Buchnera PG in vitro, and interrogate PG gene functions in vivo, implementing novel genetic
tools for the aphid-Buchnera system. We predict that aphids use PG genes to disrupt Buchnera PG recycling
and halt cell division, enabling hosts to control symbiont abundance by negative regulation. Our genome-scale
approaches will enable discovery of other potential genetic bases of symbiont control. Results of the proposed
work will contribute significantly to our understanding of how animals interact with symbiotic bacteria and, more
specifically, how hosts regulate symbionts. These findings may lead to novel drugs targeting bacterial
symbionts of insect disease vectors, or ...

## Key facts

- **NIH application ID:** 10228362
- **Project number:** 3F32GM126706-03S1
- **Recipient organization:** UNIVERSITY OF TEXAS AT AUSTIN
- **Principal Investigator:** Thomas E Smith
- **Activity code:** F32 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2020
- **Award amount:** $17,327
- **Award type:** 3
- **Project period:** 2017-09-09 → 2020-12-08

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10228362

## Citation

> US National Institutes of Health, RePORTER application 10228362, Investigations of the role of host controlled peptidoglycan recycling in the regulation of the pea aphid-Buchnera symbiosis (3F32GM126706-03S1). Retrieved via AI Analytics 2026-05-23 from https://api.ai-analytics.org/grant/nih/10228362. Licensed CC0.

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