BIG regulates stomatal immunity and jasmonate production in Arabidopsis.

Plants have evolved an array of responses that provide them with protection from attack by microorganisms and other predators. Many of these mechanisms depend upon interactions between the plant hormones jasmonate (JA) and ethylene (ET). However, the molecular basis of these interactions is insufficiently understood. Gene expression and physiological assays with mutants were performed to investigate the role of Arabidopsis BIG gene in stress responses. BIG transcription is downregulated by methyl JA (MeJA), necrotrophic infection or mechanical injury. BIG deficiency promotes JA-dependent gene induction, increases JA production but restricts the accumulation of both ET and salicylic acid. JA-induced anthocyanin accumulation and chlorophyll degradation are enhanced and stomatal immunity is impaired by BIG disruption. Bacteria- and lipopolysaccaride (LPS)-induced stomatal closure is reduced in BIG gene mutants, which are hyper-susceptible to microbial pathogens with different lifestyles, but these mutants are less attractive to phytophagous insects. Our results indicate that BIG negatively and positively regulate the MYC2 and ERF1 arms of the JA signalling pathway. BIG warrants recognition as a new and distinct regulator that regulates JA responses, the synergistic interactions of JA and ET, and other hormonal interactions that reconcile the growth and defense dilemma in Arabidopsis.

Rice BIG gene is required for seedling viability.

Arabidopsis BIG (AtBIG) gene encodes an enormous protein that is required for auxin transport. Loss of AtBIG function not only profoundly changes plant architecture but also alters plant adaptability to environmental stimuli. A putative homolog of AtBIG exists in the rice genome, but no function has been ascribed to it. In this study, we focus on the characterization of the gene structure and function of OsBIG. Sequence and phylogenetic analysis shows that the homologs of OsBIG have high amino acid conservation in several domains across species. Transgenic rice plants in which the expression of OsBIG was disrupted through the CRISPR/Cas9 system-mediated genome editing were used for phenotypic analysis. The Osbig/- plants show high levels of cell death, enhanced electrolyte leakage and membrane lipid peroxidation, and reduced chlorophyll content, which likely accounted for the seedling lethality. Moreover, gene expression between Osbig/- and wild-type plants analyzed by RNA-seq indicates that a number of metabolic and hormonal pathways including ribosome, DNA replication, photosynthesis, and chlorophyll metabolism were significantly perturbed by OsBIG deficiency. In summary, OsBIG gene is integral to the normal growth and development in rice.

The BIG protein distinguishes the process of CO2 -induced stomatal closure from the inhibition of stomatal opening by CO2.

We conducted an infrared thermal imaging-based genetic screen to identify Arabidopsis mutants displaying aberrant stomatal behavior in response to elevated concentrations of CO2 . This approach resulted in the isolation of a novel allele of the Arabidopsis BIG locus (At3g02260) that we have called CO2 insensitive 1 (cis1). BIG mutants are compromised in elevated CO2 -induced stomatal closure and bicarbonate activation of S-type anion channel currents. In contrast with the wild-type, they fail to exhibit reductions in stomatal density and index when grown in elevated CO2 . However, like the wild-type, BIG mutants display inhibition of stomatal opening when exposed to elevated CO2 . BIG mutants also display wild-type stomatal aperture responses to the closure-inducing stimulus abscisic acid (ABA). Our results indicate that BIG is a signaling component involved in the elevated CO2 -mediated control of stomatal development. In the control of stomatal aperture by CO2 , BIG is only required in elevated CO2 -induced closure and not in the inhibition of stomatal opening by this environmental signal. These data show that, at the molecular level, the CO2 -mediated inhibition of opening and promotion of stomatal closure signaling pathways are separable and BIG represents a distinguishing element in these two CO2 -mediated responses.