Sphingolipid biosynthesis modulates plasmodesmal ultrastructure and phloem unloading

TL;DR

This study uncovers how sphingolipid biosynthesis influences plasmodesmal structure and function, affecting cell-to-cell transport during phloem unloading in plants, revealing new insights into plant vascular biology.

Contribution

It identifies a novel gene, PLM, linking sphingolipid biosynthesis to plasmodesmal ultrastructure and post-sieve element unloading regulation.

Findings

PLM gene encodes a sphingolipid biosynthesis enzyme.

Loss of PLM enhances symplastic transport at specific interfaces.

Sphingolipid metabolism affects plasmodesmal ultrastructure and function.

Abstract

During phloem unloading, multiple cell-to-cell transport events move organic substances to the root meristem. Although the primary unloading event from the sieve elements to the phloem pole pericycle has been characterized to some extent, little is known about post-sieve element unloading. Here, we report a novel gene, PHLOEM UNLOADING MODULATOR (PLM), in the absence of which plasmodesmata-mediated symplastic transport through the phloem pole pericycle--endodermis interface is specifically enhanced. Increased unloading is attributable to a defect in the formation of the endoplasmic reticulum--plasma membrane tethers during plasmodesmal morphogenesis, resulting in the majority of pores lacking a visible cytoplasmic sleeve. PLM encodes a putative enzyme required for the biosynthesis of sphingolipids with very-long-chain fatty acid. Taken together, our results indicate that post-sieve element unloading involves sphingolipid metabolism, which affects plasmodesmal ultrastructure. They also raise the question of how and why plasmodesmata with no cytoplasmic sleeve facilitate molecular trafficking.