# Administrative Supplement for Equipment Related to Mechanical Regulation of Apical and Invasive Growth

> **NIH NIH R01** · UNIVERSITY OF CALIFORNIA RIVERSIDE · 2020 · $60,000

## Abstract

RESEARCH STRATEGY
Abstract
Retrograde signaling is an essential organelles-to-nucleus communication pathway, central to
maintenance of cellular homoeostasis in response to developmental and environmental inputs. We
have identified the first stress-specific plastid-to-nucleus retrograde signaling metabolite,
methylerythritol cyclodiphosphate (MEcPP), an isoprenoid precursor produced by the non-mevalonate
methylerythritol phosphate (MEP) pathway. This is a conserved signaling pathway present in plants,
pathogenic bacteria and the parasite, malaria, but absent in animals. As such, it has provided a
validated target for the development of antibacterial and antimalarial agents. The long-term goal of our
research is to delineate the perception and signal transduction components of MEcPP-mediated
signaling cascade. This competitive renewal proposal specifically aims at delineating: 1) Cellular
components of the MEcPP retrograde signaling pathway. To identify the components responsible
for the perception and transduction of the MEcPP signal, we will initially characterize the mutated
genes in the two classes of suppressor lines that, despite their equally constitutively elevated MEcPP
levels, are either almost fully or only partially incapable of inducing MEcPP response genes.
Systematic characterization of these perception/signaling network components will provide
fundamental information regarding the underlying molecular mechanisms that link a single retrograde
signaling molecule, MEcPP, to its targeted ensemble of genes. 2). Molecular link between MEcPP
and unfolded protein response in the ER. Combined global transcriptome and proteome profiling,
together with molecular genetics and pharmacological approaches, has enabled us to identify MEcPP
as an inducer of the Unfolded Protein Response (UPR) in the endoplasmic reticulum (ER). We will
decipher the MEcPP mechanism of action in induction of the UPR, and conversely delineate the role
of the UPR in MEcPP-mediated responses. This finding ushers novel insight into uncharted territories
of interorganellar signaling, and will provide a deeper understanding of key role of UPR in controlling
principal mechanisms supporting robustness. 3). Governing components of stromule formation
Imaging analyses of plants expressing a construct containing three chimeric marker genes that label
plastids with CFP, ER with YFP, and the nucleus with mCherry, has established a direct correlation
between enhanced MEcPP levels and increased presence of induced dynamic chloroplast tubular
extensions called "stromules”, that extend from plastids to ER to nucleus. We will perform
comparative proteomic analyses of genotypes with varying numbers of stromules to identify cellular
machineries responsible for their formation and to test the potential role of stromules as
communication conduits.

## Key facts

- **NIH application ID:** 10135739
- **Project number:** 3R01GM107311-07S1
- **Recipient organization:** UNIVERSITY OF CALIFORNIA RIVERSIDE
- **Principal Investigator:** KATAYOON DEHESH
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2020
- **Award amount:** $60,000
- **Award type:** 3
- **Project period:** 2013-09-05 → 2022-02-28

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10135739

## Citation

> US National Institutes of Health, RePORTER application 10135739, Administrative Supplement for Equipment Related to Mechanical Regulation of Apical and Invasive Growth (3R01GM107311-07S1). Retrieved via AI Analytics 2026-07-25 from https://api.ai-analytics.org/grant/nih/10135739. Licensed CC0.

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