Auxin analog-induced Ca(2+) signaling is not involved in inhibition of endosomal aggregation

Much of what we know about the role of auxin in plant development derives from exogenous manipulations of auxin distribution and signaling, using inhibitors, auxins and auxin analogs. In this context, synthetic auxin analogs, such as 1-Naphtalene Acetic Acid (1-NAA), are often favored over the endogenous auxin indole-3-acetic acid (IAA), in part due to their higher stability. While such auxin analogs have proven to be instrumental to reveal the various faces of auxin, they displays in some cases distinct bioactivities compared to IAA. Here, we focused on the effect of auxin analogs on the accumulation of PIN proteins in Brefeldin A (BFA)-sensitive endosomal aggregations (BFA bodies), and the correlation with the ability to elicit Ca(2+) responses. For a set of commonly used auxin analogs, we evaluated if auxin-analog induced Ca(2+) signaling inhibits PIN accumulation in. We found that not all auxin analogs elicited a Ca(2+) response, and that their differential ability to elicit Ca(2+) responses correlated partially with their ability to inhibit BFA-body formation. However, in tir1/afb and cngc14, 1-NAA-induced Ca(2+) signaling was strongly impaired, while 1-NAA’s still could inhibit PIN accumulation in BFA bodies. This demonstrates that TIR1/AFB-CNGC14-dependent Ca(2+) signaling does not inhibit BFA body formation.