The SNARE protein LbSYP61 participates in salt secretion in Limonium bicolor

Soil salinization is a global problem that inhibits plant growth and limits crop production. Recretohalophyte plants secrete excess salt via salt glands, thus avoiding excessive accumulation of salt within their cells and protecting themselves from salt-associated damage. However, the molecular mechanisms underlying salt secretion via salt glands are unclear. Here, we used brefeldin A (BFA), a specific inhibitor of Golgi-mediated cell secretion, to test whether vesicle transport participates in salt secretion in the recretohalophyte Limonium bicolor using leaf disc and non-invasive micrometric assays. Indeed, salt secretion via salt glands was significantly inhibited, the Golgi apparatus in the salt gland was damaged, and acidic phosphatase activity was significantly inhibited following a 200 μg/ml BFA treatment. To further examine the role of vesicle transport in salt secretion, we used virus-induced gene silencing (VIGS) to downregulate the gene encoding a trans Golgi-localized soluble N-ethylmaleimide-sensitive factor attachment protein receptor (SNARE) protein, LbSYP61. After silencing LbSYP61, the ability of L. bicolor to secrete salt via salt glands was also significantly reduced. These results provide direct evidence that vesicular transport participates in salt secretion via salt glands and the vesicular transport-related protein LbSYP61 plays an important role in this process.