# RO1NS118020 Research Supplements to Promote Diversity in Health-Related Research

> **NIH NIH R01** · RUTGERS THE STATE UNIV OF NJ NEWARK · 2022 · $62,188

## Abstract

ABSTRACT
 Cells have a limited capacity to synthesize choline, thus cells depend on protein transporters to import
choline. Choline is used to synthesize phosphatidylcholine, from which structural lipid components of myelin are
synthesized. Phosphatidylcholine is also metabolized to generate phosphotidylinositols, whose phosphorylated
derivatives are important signaling lipids that regulate myelination. Choline is involved in synthesis of the
universal methyl donor, S-adenosylmethionine (SAM) for histone and DNA methylation, thus regulating gene
expression. Considering the position of choline at the crossroad for the biosynthesis of phospholipids and
epigenetic regulation, we have very little to no understanding of the regulation of choline import and choline-
dependent metabolism in myelinating glial cells. Choline transporters for myelin-forming glial cells have not been
identified.
 We have identified choline-like-transporter 1 (CTL1) as an important regulator of Schwann cell myelination.
CTL1 deletion in Schwann cells (CTL1sc-KO) results in early onset of focal hyper-myelination in the PNS.
Biochemical analysis revealed an overall decrease in choline-derived phospholipids in the myelin. Furthermore,
CTL1 loss impaired myelin gene expression and exhibited altered DNA modifications in Schwann cells. Parent
grant proposal of this supplement test the hypothesis that CTL1 is a Schwann cell choline transporter. To that
end, we are currently testing three aims to determine: 1) whether CTL1 functions as a choline transporter in
Schwann cells, 2) whether CTL1 contributes to phosphatidylinositol signaling in the PNS and 3) whether CTL1
loss impact genetic and epigenetic profiles in Schwann cells.
 Using the available tools and experimental techniques from the parent study, the proposed study in this
Research Supplement is designed to test the hypothesis that CTL1 functions as a choline transporter in
oligodendrocytes. This is based on previous reports and our recent findings that CTL1 is highly expressed in
oligodendrocytes and its expression increased during oligodendrocyte differentiation. Ms Adriana Torres, who
will be supported on the supplement funds, will carry on two specific aims that will determine 1) whether CTL1
functions as a choline transporter in oligodendrocytes and 2) whether CTL1-deficiency in vivo impacts
oligodendrocyte development and myelination. Results from the study are expected to provide important insights
into understanding the function of choline transport and its metabolism in myelin-forming glial cells.

## Key facts

- **NIH application ID:** 10622090
- **Project number:** 3R01NS118020-03S1
- **Recipient organization:** RUTGERS THE STATE UNIV OF NJ NEWARK
- **Principal Investigator:** HAESUN A KIM
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2022
- **Award amount:** $62,188
- **Award type:** 3
- **Project period:** 2020-09-01 → 2025-05-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10622090

## Citation

> US National Institutes of Health, RePORTER application 10622090, RO1NS118020 Research Supplements to Promote Diversity in Health-Related Research (3R01NS118020-03S1). Retrieved via AI Analytics 2026-05-27 from https://api.ai-analytics.org/grant/nih/10622090. Licensed CC0.

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