Sortinl Disrupts Vacuolar Trafficking of both Proteins and Flavonoids

Sortinl Disrupts Vacuolar Trafficking of both Proteins and Flavonoids 

Sortinl affects the vacuolar trafficking of both proteins and flavonoids, indicating that flavonoid transport to the vacuole could share the same membrane-mediated pathway as vacuolar proteins. But this does not rule out the possibility that one of the trafficking defects is direct, whereas the other one is indirect. The fact that Sortinl mimics BSO to produce an oxidized cell environment to affect ABC transporter activity supports a model that a transporter-mediated flavonoid transport defect induces miss-trafficking of other vacuolar contents such as the proteins. On the other hand, mutants defective in flavonoid metabolism, such as tt4, show hypersensitivity to Sortinl and have altered vacuolar morphology 

Sortinl decomposes in plant growth media where one of the products resembles the effects of BSO, a GSH biosynthesis inhibitor. This indicates that a series of observed Sortinl effects might be due to an oxidized cellular environment that it creates. It could be that Sortinl or an active decomposition product sequesters GSH or inhibits GSH production. This may induce the transcription of cytochrome P450-dependent monooxygenases and mixed function oxidases, as shown in the transcription profile after Sortinl treatment. Reduced GSH level then affects flavonoid transport. 

The mechanism of flavonoid regulation of vacuolar biogenesis is not understood. However, the existence of vacuole biogenesis and flavonoid accumulation phenotypes in different mutants, such as mtv6, ahalO, ttl2, and tds4 [9, 10, 16, 

17] indicates that there is a connection between the two pathways. Sortinl might serve as a tool in solving this question. 

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