**1. Introduction**

A water deficit is a restrictive factor for plant development, productivity, and geographical distribution. Plants have evolved varied strategies to cope with decreased water availability, including promoting stomatal closure and altered plant growth and development. The stress-induced hormone abscisic acid (ABA) plays an important role in a plant's response to drought tolerance [1–3]. Increasing evidence has proven that gibberellin (GA) plays a negative role in drought response. The over-accumulation of the GA mutant or increased GA activity shows an increased water deficit sensitivity, whereas a GA-deficient mutant or decreased GA activity shows an increased water deficit tolerance [4–8].

DELLA (GAI/RGA/RGL1/RGL2/RGL3) proteins are major negative regulators of GA signaling. In the absence of GA, DELLA proteins inhibit the GA-dependent processes, including germination, growth, and flowering. Under increased GA levels, GA binds to its nuclear receptor GID1 (GA insensitive dwarf1) and changes its conformation, leading to its interaction with the N-terminal end of DELLA proteins [9–11]. The interaction of DELLA proteins with GID1 causes its ubiquitination and subsequent degradation by the 26S proteasome, leading to the activation of GA responses [12,13]. DELLA proteins

are involved in most GA-mediated plant growth and environmental stresses, including dehydration stress. Recently, it was reported that the DELLA protein PRO (PROCERA) in tomato functions positively in the plant response to drought stress. The loss-of-function of the *PRO* mutant shows a reduced tolerance to drought, whereas the overexpression of the constitutively active stable *PRO* increases drought tolerance [8]. However, the molecular mechanism of DELLA proteins remains unclear.

There are five DELLA members in Arabidopsis: GAI (GA INSENSITIVE), RGA (REPRESSOR OR GAI3), RGL1 (RGA-LIKE1), RGL2, and RGL3. To uncover the molecular mechanism that determines how DELLA proteins function in drought tolerance, we used GAI as a sample to analyze the function of DELLA proteins in response to drought stress. We made use of a gain-of-function mutant *gai-1* generated from the *gai*-*1* (L*er*) allele (with a 17 amino acid deletion within the DELLA domain of GAI) by backcrossing *gai*-*1* (L*er*) with Col-0 (Columbia-0) three times. We showed that this mutant has an increased drought tolerance phenotype. Further, we found that GAI and other DELLA proteins interacted with ABF2 (abscisic acid (ABA)-responsive element (ABRE)-binding transcription factors), the transcriptional factor that plays a pivotal role in ABA signaling for drought tolerance. Our results thus shed some light on the mechanism behind how DELLA proteins function in drought stress tolerance.
