Plants balance their competing requirements for growth and stress tolerance via a sophisticated regulatory circuitry that controls responses to the external environments. We have identified a plant-specific gene, COST1 ( constitutively stressed 1 ), that is required for normal plant growth but negatively regulates drought resistance by influencing the autophagy pathway. An Arabidopsis thaliana cost1 mutant has decreased growth and increased drought tolerance, together with constitutive autophagy and increased expression of drought-response genes, while overexpression of COST1 confers drought hypersensitivity and reduced autophagy. The COST1 protein is degraded upon plant dehydration, and this degradation is reduced upon treatment with inhibitors of the 26S proteasome or autophagy pathways. The drought resistance of a cost1 mutant is dependent on an active autophagy pathway, but independent of other known drought signaling pathways, indicating that COST1 acts through regulation of autophagy. In addition, COST1 colocalizes to autophagosomes with the autophagosome marker ATG8e and the autophagy adaptor NBR1, and affects the level of ATG8e protein through physical interaction with ATG8e, indicating a pivotal role in direct regulation of autophagy. We propose a model in which COST1 represses autophagy under optimal conditions, thus allowing plant growth. Under drought, COST1 is degraded, enabling activation of autophagy and suppression of growth to enhance drought tolerance. Our research places COST1 as an important regulator controlling the balance between growth and stress responses via the direct regulation of autophagy.

Summary: Brassinosteroids (BRs) are essential hormones that play crucial roles in plant growth, reproduction and response to abiotic and biotic stress. In Arabidopsis, AtCYP85A2 works as a bifunctional cytochrome P450 monooxygenase to catalyse the conversion of castasterone to brassinolide, a final rate‐limiting step in the BR‐biosynthetic pathway. Here, we report the functional characterizations of PtCYP85A3, one of the three AtCYP85A2 homologous genes from Populus trichocarpa. PtCYP85A3 shares the highest similarity with AtCYP85A2 and can rescue the retarded‐growth phenotype of the Arabidopsis cyp85a2‐2 and tomato d^x mutants. Constitutive expression of PtCYP85A3, driven by the cauliflower mosaic virus 35S promoter, increased the endogenous BR levels and significantly promoted the growth and biomass production in both transgenic tomato and poplar. Compared to the wild type, plant height, shoot fresh weight and fruit yield increased 50%, 56% and 43%, respectively, in transgenic tomato plants. Similarly, plant height and stem diameter increased 15% and 25%, respectively, in transgenic poplar plants. Further study revealed that overexpression of PtCYP85A3 enhanced xylem formation without affecting the composition of cellulose and lignin, as well as the cell wall thickness in transgenic poplar. Our finding suggests that PtCYP85A3 could be used as a potential candidate gene for engineering fast‐growing trees with improved wood production.

Background: R2R3-MYB transcription factors (TFs) play important roles in plant growth and development, and response to biotic and abiotic stresses. However, their regulatory mechanisms in wound-induced anthocyanin biosynthesis in woody plants are largely unknown. Results: In this work, we report that expression of anthocyanin biosynthesis genes (ABGs) were activated by PdMYB118, a MYB TF encoding gene from Populus deltoids, and the activation of PdMYB118 was significantly enhanced by PdTT8, a bHLH protein, through its direct interaction with PdMYB118. PdMYB118 and some ABGs were evidently induced by wound induction and methyl jasmonate (MeJA) treatment. Overexpression of PdMYB118 promoted anthocyanin accumulation in transgenic poplar upon wound induction. Furthermore, a poplar JASMONATE ZIM-domain (JAZ) protein, PtrJAZ1, repressed the transcriptional function of PdMYB118/PdTT8 complex by binding to PdTT8, and wound stimulated the biosynthesis of jasmonic acid (JA) and the degradation of PtrJAZ1. Conclusions: Based on these observations, we proposed that PtrJAZ1 degradation triggered the expression of ABGs, leading to increased biosynthesis of anthocyanins in the wounded leaves of transgenic poplar. Therefore, our findings not only illustrate the crucial role of PdMYB118 in wound-induced anthocyanin biosynthesis in poplar, but also provide a molecular basis for the genetic engineering of colorful tree species.

Glutathione S-transferases (GSTs) play an essential role in plant cell detoxification and secondary metabolism. However, their accurate functions in the growth and response to abiotic stress in woody plants are still largely unknown. In this work, a Phi class Glutathione S-transferase encoding gene PtGSTF1 was isolated from poplar (P. trichocarpa), and its biological functions in the regulation of biomass production and salt tolerance were investigated in transgenic poplar. PtGSTF1 was ubiquitously expressed in various tissues and organs, with a predominant expression in leaves and inducible expression by salt stress. Transgenic poplar overexpressing PtGSTF1 showed improved shoot growth, wood formation and improved salt tolerance, consistent with the increased xylem cell number and size under normal condition, and the optimized Na⁺ and K⁺ homeostasis and strengthened reactive oxygen species scavenging during salt stress. Further transcriptome analyses demonstrated that the expressions of genes related to hydrolase, cell wall modification, ion homeostasis and ROS scavenging were up- or down-regulated in transgenic plants. Our findings imply that PtGSTF1 improves both biomass production and salt tolerance through regulating hydrolase activity, cell wall modification, ion homeostasis and ROS scavenging in transgenic poplar, and that it can be considered as a useful gene candidate for the genetic breeding of new tree varieties with improved growth under salt stress conditions.

Plants in the juvenile state are more tolerant to adverse conditions. Constitutive expression of MicroRNA156 (miR156) prolonged the juvenile phase and increased resistance to abiotic stress, but also affected the architecture of transgenic plants. In this study, we investigated the possibility of subtle manipulation of miR156 expression in flowering plants, with the goal to increase tolerance to abiotic stress without altering the normal growth and development of transgenic plants. Transgenic tobacco plants expressing ZmmiR156 from maize were generated, driven either by the cauliflower mosaic virus (CaMV) 35S promoter or the stress-inducible ZmRab17 promoter. Expression of ZmmiR156 led to improved drought and salt tolerance in both 35S::MIR156 and Rab17::MIR156 transgenic plants, as shown by more vigorous growth, greater biomass production and higher antioxidant enzyme expression after a long period of drought or salt treatment, when compared to wild type and transgenic vector control plants. However, constitutive expression of ZmmiR156 also resulted in retarded growth, increased branching and delayed flowering of transgenic plants. These undesirable developmental changes could be mitigated by using the stress-inducible ZmRab17 promoter. Furthermore, under drought or salt stress conditions, expression of ZmmiR156 reduced the transcript level of NtSPL2 and NtSPL9, the genes potentially targeted by ZmmiR156, as well as that of CP1, CP2, and SAG12, the senescence-associated genes in tobacco. Collectively, our results indicate that ZmmiR156 can be temporally manipulated for the genetic improvement of plants resistant to various abiotic stresses.