Drought is one of the most important environmental stresses affecting the productivity of most field crops. Elucidation of the complex mechanisms underlying drought resistance in crops will accelerate the development of new varieties with enhanced drought resistance. Here, we provide a brief review on the progress in genetic, genomic, and molecular studies of drought resistance in major crops. Drought resistance is regulated by numerous small-effect loci and hundreds of genes that control various morphological and physiological responses to drought. This review focuses on recent studies of genes that have been well characterized as affecting drought resistance and genes that have been successfully engineered in staple crops. We propose that one significant challenge will be to unravel the complex mechanisms of drought resistance in crops through more intensive and integrative studies in order to find key functional components or machineries that can be used as tools for engineering and breeding drought-resistant crops.

Dark respiration causes an increase in the leaf CO2 concentration (Ci) and the continuing atmospheric [CO2] rise further increases Ci. Elevated Ci causes closing of stomatal pores, thus regulating plant gas exchange. The molecular signaling mechanisms leading to CO2-induced stomatal closure are only partially understood. Here we demonstrate that high intracellular CO2/HCO3- enhances currents mediated by the guard cell S-type anion channel SLAC1 when co-expressing either of the protein kinases OST1, CPK6 or CPK23 in Xenopus oocytes. Split-ubiquitin screening identified the PIP2;1 aquaporin as an interactor of the βCA4 carbonic anhydrase, which was confirmed in split luciferase, bimolecular fluorescence complementation and co-immunoprecipitation experiments. PIP2;1 exhibited CO2-permeability. Mutation of PIP2;1 in planta alone was insufficient to impair CO2- and ABA-induced stomatal closing likely due to redundancy. Interestingly, co-expression of βCA4 and PIP2;1 with OST1-SLAC1 or CPK6/23-SLAC1 in oocytes enabled extracellular CO2 enhancement of SLAC1 anion channel activity. An inactive PIP2;1 point mutation was identified which abrogated water and CO2 permeability and extracellular CO2 regulation of SLAC1 activity. These findings identify the CO2-permeable PIP2;1 as key interactor of βCA4 and show functional reconstitution of extracellular CO2 signaling to ion channel regulation upon co-expression of PIP2;1, βCA4, SLAC1 and protein kinases. These findings further implicate SLAC1 as a bicarbonate-responsive protein contributing to CO2 regulation of S-type anion channels.

Intracellular targeting of guard cell carbonic anhydrases is characterized and modeled in relation to their roles in CO2 control of stomatal movements.

High salinity is one of the major environmental stresses that plants encounter. Roots are the initial and direct organs to perceive the signal. However, how plant roots perceive and respond to salinity at the molecular and physiological levels is still poorly understood. Here, we report that IAA-CONJUGATE-RESISTANT 4 (IAR4) plays a key role in primary root growth under salt stress conditions. Mutation of IAR4 led to increased sensitivity to salt stress conditions, with strongly inhibited primary root growth and reduced survival rate in two iar4 mutant alleles. iar4 mutants accumulated greater Na⁺ and exhibited a greater Na⁺/K⁺ ratio under NaCl treatment. In addition, more reactive oxygen species (ROS) accumulated in the iar4 mutants due to reduced ROS scavenging. NaCl treatment greatly suppressed the expression levels of ProPIN1:PIN1-GFP, ProPIN2:PIN2-GFP, ProPIN3:PIN3-GFP, and ProDR5:GFP, and suppressed root meristem activity in iar4. GSH or auxin treatment greatly recovered the PIN expression, auxin distribution and primary root growth in the iar4 mutants, suggesting ROS is a vital mediator between salt stress and auxin response. Our data support a model in which IAR4 integrates ROS and auxin pathways to modulate primary root growth under salinity stress conditions, by regulation of PIN-mediated auxin transport.

Abscisic acid (ABA)-activated inward Ca²⁺-permeable channels in the plasma membrane (PM) of guard cells are required for the initiation and regulation of ABA-specific cytosolic Ca²⁺ signaling and stomatal closure in plants. But the identities of the PM Ca²⁺ channels are still unknown. We hypothesized that the ABA-activated Ca²⁺ channels consist of multiple CYCLIC NUCLEOTIDE-GATED CHANNEL (CNGC) proteins from the CNGC family, which is known as a Ca²⁺-permeable channel family in Arabidopsis (Arabidopsis thaliana). In this research, we observed high expression of multiple CNGC genes in Arabidopsis guard cells, namely CNGC5, CNGC6, CNGC9, and CNGC12. The T-DNA insertional loss-of-function quadruple mutant cngc5-1 cngc6-2 cngc9-1 cngc12-1 (hereafter c5/6/9/12) showed a strong ABA-insensitive phenotype of stomatal closure. Further analysis revealed that ABA-activated Ca²⁺ channel currents were impaired, and ABA-specific cytosolic Ca²⁺ oscillation patterns were disrupted in c5/6/9/12 guard cells compared with in wild-type guard cells. All ABA-related phenotypes of the c5/6/9/12 mutant were successfully rescued by the expression of a single gene out of the four CNGCs under the respective native promoter. Thus, our findings reveal a type of ABA-activated PM Ca²⁺ channel comprising multiple CNGCs, which is essential for ABA-specific Ca²⁺ signaling of guard cells and ABA-induced stomatal closure in Arabidopsis.