**6. Conclusions**

In this review, we examined a key finding, recently reported by Fàbregas and colleagues [2], in which an increased expression of the BRL3 receptor provided resistance to a lack of water but did not impair plant development. Such cases, in relation to any stress, are quite rare, since resistance to any stressful condition is usually accompanied by growth retardation. Drought tolerance of plants is controlled by numerous signaling modules forming a branched network of protein–protein interactions. In this study, we examined all known interactions of the BR and ABA signaling pathways, but left out the signaling pathways of gibberellins and the light signaling system, which undoubtedly a ffect stress tolerance, but would greatly complicate the understanding of the described phenomenon.

In such cases as the one that was described by Fàbregas et al. [2], we should look for adaptation processes caused by memory generation. Ding et al. [39] postulated that under natural conditions, stress memory is activated by the previous dehydration stress, continues during the recovery period, and prepares the plant's response to the next dehydration stress. This is surprising, but so far the

BR pathway has not been extensively studied with respect to epigenetic changes and the generation of stress memory, and only the first steps have been taken on this path [45–47,68,71]. For the closest animal relatives of BRs, glucocorticoids, we observe an extensive field of research related specifically to changes in chromatin structure [72]. At present, it is still unclear whether BRs have a lesser e ffect on adaptive chromatin rearrangements or if they are simply underexplored in this regard.

We hypothesized that BRs may be involved in stress acclimation by three interconnected mechanisms. The first mechanism is that the signal passes through the module BRL3 (or BRI1) → BSK1/3 → BSU1 — BIN2 → BSK1/3, in which BIN2 is responsible for communication with ABA signaling and the BSK proteins serve as signal concentrators. The second mechanism is priming through chromatin modifications, in which BRL3 and other BR receptors could act collectively to ensure stress memory via BIN2 → SnRK2s → ABF2, BES1 or BZR1–TPL –HDA19 repressor complexes and BZR1/BES1 → FLC/FCA pathway. The third mechanism is stress acclimation by the BR-mediated stabilization of endoplasmic proteins in the ERAD process. New research prospects involving the BR signaling pathway in relation to stress adaptation are very intriguing and include the study of BR and ABA interaction pathways, chromatin modifications, and the ERAD process.

**Author Contributions:** Conception, data analysis, manuscript writing, V.P.B.; analysis and interpretation of data, revising for important intellectual content, final approval, T.V.A. All authors have read and agreed to the published version of the manuscript.

**Funding:** This research was funded by the Russian Science Foundation, gran<sup>t</sup> number 18-44-08001 (VPB).

**Conflicts of Interest:** The authors declare no conflict of interest.
