LMBD2 interacts with components of the ECH/YIP complex and contributes to post-Golgi trafficking in Arabidopsis.

Abstract

The plant cell wall, composed primarily of polysaccharides, is essential for normal plant growth and development. Many of these polysaccharides are synthesized within and subsequently secreted via the endomembrane system. Mutations in genes including MURUS3 (MUR3), YPT/RAB GTPase-interacting protein 4 homologs (YIP4a/YIP4b), and ECHIDNA (ECH) result in dwarf plants, which is believed to be a consequence of impaired cell wall polysaccharide secretion. Here, we identify a LMBR1 (Limb Development Membrane Protein 1)-like membrane protein (LMBD2) and find that loss of LMBD2 suppresses the secretion and growth defects in the mur3, yip4a yip4b, and ech mutants. LMBD2 localizes to the trans-Golgi apparatus and trans-Golgi network/early endosome, where it interacts with YIP4b and orchestrates trans-Golgi network/early endosome-mediated trafficking. Furthermore, LMBD2 can competitively attenuate the interaction of YIP4b and ECH. Our findings establish LMBD2 as a component of endomembrane trafficking homeostasis in plant cells and offer new insights into endomembrane dynamics and their influence on plant development.