# Integrated transcriptomic and metabolomic analyses reveal flavonoid and lipid metabolic reprogramming in Dendrobiumofficinale during Colletotrichum fructicola-induced anthracnose

## TL;DR

This study explores how the medicinal plant Dendrobium officinale changes its metabolism in response to a fungal infection, revealing key pathways involved in defense.

## Contribution

The study identifies a novel metabolic axis linking lipid catabolism to flavonoid biosynthesis during pathogen infection in Dendrobium officinale.

## Key findings

- Pathogen infection upregulates flavonoid biosynthesis genes like DFR and LDOX in Dendrobium officinale.
- Lipid catabolism increases, with elevated free fatty acids and reduced phospholipids like PC and PE.
- Acyl-CoA intermediates connect lipid breakdown to flavonoid production, suggesting a defense-related metabolic pathway.

## Abstract

Anthracnose disease caused by Colletotrichum fructicola severely compromises the medicinal value and yield of Dendrobium officinale. To elucidate the host metabolic response to pathogen infection, we integrated transcriptomic and metabolomic analyses of D. officinale challenged with C. fructicola. Our results revealed a profound metabolic reprogramming orchestrated by the pathogen, characterized by upregulated flavonoid biosynthesis (e.g., DFR, LDOX activation) and enhanced lipid catabolism (e.g., β-oxidation via LACS, DECR, HACL). Metabolite profiling demonstrated a significant reduction in phosphatidylcholine (PC) and phosphatidylethanolamine (PE) alongside increased free fatty acids, indicating active lipid degradation. Notably, acyl-CoA intermediates linked lipid catabolism to flavonoid production, suggesting a metabolic axis where pathogen-induced lipid breakdown fuels defense-related secondary metabolite synthesis. This study identifies flavonoid and lipid metabolic reprogramming as critical axes in host-pathogen interactions, providing a foundation for developing targeted disease control strategies.