A new regulator of vesicle trafficking in plants

The protein, called choline transporter-like 1 (CTL1), had been previously identified as essential for formation of sieve plates, cell wall perforations that regulate passage of materials in plant phloem. But the mechanism of its function, and whether it played other roles in plants, was unknown. Chao and colleagues found CTL1 while screening for genes that control ion homeostasis in the model plant, Arabidopsis thaliana. They found that loss of CTL1 in the root led to ion disturbances in leaves, and deformations in plasmodesmata, a type of intercellular channel, in the root. CTL1 mutation also altered the distribution of ion transporters, which, combined with previous work localizing CTL1 to the trans-Golgi network, led the authors to investigate whether CTL1 played a direct role in vesicle trafficking. Sure enough, they showed that loss of CTL1 disrupted localization of multiple proteins, including an auxin transporter -- auxin is the main growth hormone in plants.

Luan and colleagues began by mapping the distribution of CTL1 in Arabidopsis, and found that it was ubiquitous but was highest where auxin was highest: in the growing tips, in the vascular tissue, and in the "apical hook" that seedlings lead with as they push up through the soil. Intracellularly, they too found that CTL1 localized to the trans-Golgi network, and appeared to control trafficking to and from the plasma membrane; the authors observed that without CTL1, auxin transporters were misdirected, and the plant displayed the classic signs of auxin loss, including lack of cell elongation.

Chao also showed that excess choline inhibited endocytosis, mimicking the effects of CTL1 loss and suggesting that a critical CTL1 function is to sequester choline into endosomes. They suggest that keeping choline levels low outside endosomes promotes the activity of an enzyme, phospholipase D, that cleaves multiple lipids and, in so doing, has a direct effect on vesicle lipid composition and thus destination. In this model, loss of CTL1 raises choline, which inhibits the enzyme, altering vesicle lipids, and ultimately misdirecting the vesicles, which would account for the multiple effects of CTL1 mutation, including ion imbalances, plasmodesmata defects, and auxin mislocalization.

CTL1 is also found in animal cells, Chao noted, and thus the study concluded that "characterizing CTL1 as a new regulator of protein sorting may enable researchers to understand not only ion homeostasis in plants but vesicle trafficking in general."