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Mechanisms of Auxin-dependent Signaling in the Endoplasmic Reticulum

Periodic Reporting for period 4 - AuxinER (Mechanisms of Auxin-dependent Signaling in the Endoplasmic Reticulum)

Reporting period: 2019-12-01 to 2020-11-30

According to the Food and Agriculture Organization of the United Nations (State of Food Insecurity in the World, FAO, 2013) 842 million people have insufficient access to food, evoking hunger to the world biggest health risk. Even when hunger is low, under nutrition is causing health, social and economic problems ( Hence, knowledge on plant growth and development will have increasing significance for food safety and other socio-economic challenges. In this ERC funded research, we have assessed how the plant hormone auxin impacts on plant growth and development. We focused hereby on its subcellular regulation at the endoplasmic reticulum. The canonical auxin receptor TIR1 resides in the nucleus, where it will initiate auxin-dependent gene regulation. We have unravelled a novel auxin transport facilitator family called the PIN-LIKES (PILS). PILS proteins reside in the endoplasmic reticulum (ER), where they negatively impact on nuclear auxin signalling. In the course of this project, we have illustrated that PILS proteins limit the abundance of auxin in the nucleus, proposing that auxin compartmentalisation into the ER, prevents auxin diffusion into the nucleus. Accordingly, PILS proteins define cell type specific sensitivity to auxin. We illustrated that environmental signals, such as light and temperature, but also internal signals, such as the phytohormone brassinosteroid, modulate the transcription and protein abundance of PILS proteins, allowing to adapt auxin-dependent organ growth rates. Our work highlights the importance of the ER for auxin-dependent adaptive growth responses. The uncovered mechanism modulate adaptive plant growth responses and are interesting entry points to engineer plant performance under specific growth conditions.
The main research objective was to unravel the importance of the endoplasmic reticulum (ER) for genomic auxin responses. The PIN-LIKES (PILS) putative carriers for auxinic compounds localize to the ER, where they determine the cellular sensitivity to auxin (Barbez et al., 2012). I furthermore proposed to use the apical hook development as a model for differential growth control in plants. The apical hook is a dark grown, protective structure, showing asymmetric repression (during the formation) and promotion of growth (during opening). Using this system, we could reveal a role of PILS-dependent reduction in auxin signalling for growth induction in apical hooks (Beziat et al., 2017). We assume that PILS proteins transport auxin into the ER, thereby reducing auxin diffusion into the nucleus. In agreement, PILS proteins do reduce the abundance of nuclear auxin (Feraru et al., 2018 preprint). This work reveals that PILS proteins do not only affect auxin homeostasis (Barbez et al., 2012), but have a developmental role in controlling growth by depleting nuclear abundance (Feraru et al., 2018 preprint) and consequently signalling of auxin (Beziat et al., 2017; Feraru et al., 2018 preprint). Intriguingly, PILS proteins are utilized to integrate environmental stimuli, such as light (Beziat et al., 2017) and temperature (Feraru et al., 2018 preprint), into auxin-dependent growth programs. On the other hand, we revealed that also internal signals, such as other hormones, impact on PILS transcription (Sun et al., manuscript in preparation), suggesting that PILS proteins at the ER are important integrators of internal and external signals, modulating genomic auxin responses.
We revealed the importance of PILS proteins for auxin-dependent growth regulation by limiting nuclear availability. Along this line, PILS proteins have a developmental role by defining auxin signalling minima in the underlying tissues. This mechanism seems to be central to integrate internal and external signals into auxin-dependent growth programs. We furthermore assess the function of auxin metabolites, which also have a presumed role in reducing auxin signalling. We are currently investigating whether auxin conjugates have sole auxin storage function or whether they evolved an additional developmental role. Some components of the auxin conjugation machinery reside in the ER and, therefore, we will investigate if PILS proteins impact on this pathway. Moreover, our emerging data suggests that PILS proteins could link auxin to ER associated, basic cellular responses. We are very eager to follow this novel line of research.
Model for PILS protein-dependent reduction of nuclear auxin availability