Moulinier-Anzola, J. | Search bioRxiv

bioRxiv2026

SEC16A/MAG5-mediated ER export shapes ABA receptor homeostasis

The phytohormone abscisic acid (ABA) controls plant adaptation to environmental stress through PYR/PYL/RCAR receptors. Regulated receptor turnover through ubiquitination and endosomal trafficking, including ESCRT-dependent vacuolar degradation, is a major mechanism controlling ABA signalling. However, whether ABA receptor homeostasis is established during the early secretory pathway remains unknown. Using complementary cell biological and biochemical approaches, we define a constitutive early secretory pool of the ABA receptors PYR1 and PYL4 associated with the endoplasmic reticulum (ER) and the Golgi apparatus (GA). Genetic, cell biological and pharmacological analyses reveal that the COPII scaffold protein SEC16A (also known as MAG5) is required for the proper trafficking and homeostasis of this receptor pool. Loss of MAG5 causes intracellular receptor accumulation, impaired trafficking towards late endosomal compartments and enhanced ABA signalling without affecting endogenous ABA accumulation. Together, our findings establish the early secretory pathway as an integral component of the ABA signalling network and demonstrate that MAG5-mediated ER export shapes ABA receptor homeostasis by coordinating receptor trafficking throughout the endomembrane system, revealing the ER as a key regulatory compartment for ABA receptor homeostasis.

plant biology↗

bioRxiv2022

PILS proteins provide a homeostatic feedback on auxin signaling output

Auxin is a crucial regulator of plant growth and development. Multiple internal and external signals converge at the regulation of auxin metabolism, intercellular transport, and signaling (Pernisova and Vernoux, 2021; Anfang and Shani, 2021). Considering this complexity, it remains largely unknown how plant cells monitor and ensure the homeostasis of auxin responses. PIN-LIKES (PILS) intracellular auxin transport facilitators at the endoplasmic reticulum (ER) are suitable candidates to buffer cellular auxin responses, because they limit nuclear abundance and signaling of auxin (Barbez et al., 2012; Beziat et al., 2017; Feraru et al., 2019; Sun et al., 2020). We used forward genetics to identify mechanisms that define the PILS6 protein abundance and thereby auxin signaling outputs. We screened for gloomy and shiny pils (gasp) mutants that define the levels of PILS6-GFP under a constitutive promoter. In this study, we show that GASP1 encodes for an uncharacterized RING/U-box superfamily protein and impacts on auxin signaling output. We conclude that the low auxin signaling in gasp1 mutants correlates with reduced abundance of PILS proteins, such as PILS5 and PILS6, which consequently balances auxin-related phenotypes. In agreement, we show that high and low auxin conditions increase and reduce PILS6 protein levels, respectively. Accordingly, non-optimum auxin concentrations are buffered by alterations in PILS6 abundance, consequently leading to homeostatic auxin output regulation. We envision that this feedback mechanism provides robustness to auxin-dependent plant development.

plant biology↗