The phytohormone salicylic acid (SA) not only is a well-known signal molecule mediating plant immunity, but also is involved in plant growth regulation. However, while its role in plant immunity has been well elucidated, its action on plant growth has not been clearly described to date. Recently, increasing evidence has shown that SA plays crucial roles in regulating cell division and cell expansion, the key processes that determines the final stature of plant. This review summarizes the current knowledge on the action and molecular mechanisms through which SA regulates plant growth via multiple pathways. It is here highlighted that SA mediates growth regulation by affecting cell division and expansion. In addition, the interactions of SA with other hormones and their role in plant growth determination were also discussed. Further understanding of the mechanism underlying SA-mediated growth will be instrumental for future crop improvement.

Genome editing is widely used across plant species to generate and study the impact of functional mutations in crop improvement. However, transgene integration in plant genomes raises important legislative concerns regarding genetically modified organisms. Several strategies have been developed to remove or prevent the integration of gene editor constructs, which can be divided into three major categories: 1) elimination of transgenic sequences via genetic segregation; 2) transient editor expression from DNA vectors; and 3) DNA-independent editor delivery, including RNA or preassembled Cas9 protein-gRNA ribonucleoproteins (RNPs). Here, we summarize the main strategies employed to date and discuss the advantages and disadvantages of using these different tools. We hope that our work can provide important information concerning the value of alternative genome editing strategies to advance crop breeding.

Endoplasmic reticulum-associated degradation (ERAD) is known to regulate plant responses to diverse stresses, yet its underlying molecular mechanisms and links to various stress signaling pathways are poorly understood. Here, we show that the ERAD component ubiquitin-conjugating enzyme UBC32 positively regulates drought tolerance in Arabidopsis thaliana by targeting the aquaporins PIP2;1 and PIP2;2 for degradation. Furthermore, we demonstrate that the RING-type ligase Rma1 acts together with UBC32 and that the E2 activity of UBC32 is essential for the ubiquitination of Rma1. This complex ubiquitinates a phosphorylated form of PIP2;1 at Lys276 to promote its degradation, thereby enhancing plant drought tolerance. Extending these molecular insights into crops, we show that overexpression of Arabidopsis UBC32 also improves drought tolerance in rice (Oryza sativa). Thus, beyond uncovering the molecular basis of an ERAD-regulated stress response, our study suggests multiple potential strategies for engineering crops with improved drought tolerance.

Significance: The coreceptors of phytohormone ABA, such as ABI1, are the central regulator of plant tolerance to drought and other abiotic stresses. Tight regulation of ABI1 through ubiquitination is vital for ABA signaling and drought tolerance. In this study, we identified a mechanism to reduce ABI1 protein levels by an E2-E3 pair UBC27–AIRP3. UBC27 directly binds ABI1 and cooperates with AIRP3 in the degradation of ABI1 and ABA signaling. ABA further activates the expression of UBC27 and AIRP3 , inhibits the degradation of UBC27, and enhances the interaction between UBC27 and ABI1, establishing a positive feedback regulatory loop to control UBC27 activity under stress conditions. Our results identify a layer of ABA-pathway regulation that terminates ABI1 by the ubiquitination complex UBC27–AIRP3.