SUMMARYLow temperature is one of environmental factors that restrict plant growth homeostasis and plant-pathogen interactions. Recent studies suggest a link between temperature responses and defense responses; however, the underlying molecular mechanisms remain unclear. In this study, the chilling sensitive 3 (chs3-1) mutant in Arabidopsis was characterized. chs3-1 plants showed arrested growth and chlorosis when grown at 16°C or when shifted from 22 to 4°C. chs3-1 plants also exhibited constitutively activated defense responses at 16°C, which were alleviated at a higher temperature (22°C). Map-based cloning of CHS3 revealed that it encodes an unconventional disease resistance (R) protein belonging to the TIR-NB-LRR class with a zinc-binding LIM domain (Lin-11, Isl-1 and Mec-3 domains) at the carboxyl terminus. The chs3-1 mutation in the conserved LIMcontaining domain led to the constitutive activation of the TIR-NB-LRR domain. Consistently, the growth and defense phenotypes of chs3-1 plants were completely suppressed by eds1, sgt1b and rar1, partially by pad4 and nahG, but not by npr1 and ndr1. Intriguingly, chs3-1 plants grown at 16°C showed enhanced tolerance to freezing temperatures. This tolerance was correlated with growth defect and cell death phenotypes caused by activated defense responses. Other mutants with activated defense responses, including cpr1, cpr5 and slh1 also displayed enhanced freezing tolerance. These findings revealed a role of an unconventional mutant R gene in plant growth, defense response and cold stress, suggesting a mutual interaction between cold signaling and defense responses.

Several lipid-transfer proteins were reported to modulate the plant response to biotic stress; however, whether lipid-transfer proteins are also involved in abiotic stress remains unknown. This study characterized the function of a lipid-transfer protein, LTP3, during freezing and drought stress. LTP3 was expressed ubiquitously and the LTP3 protein was localized to the cytoplasm. A biochemical study showed that LTP3 was able to bind to lipids. Overexpression of LTP3 resulted in constitutively enhanced freezing tolerance without affecting the expression of CBFs and their target COR genes. Further analyses showed that LTP3 was positively regulated by MYB96 via the direct binding to the LTP3 promoter; consistently, transgenic plants overexpressing MYB96 exhibited enhanced freezing tolerance. This study also found that the loss-of-function mutant ltp3 was sensitive to drought stress, whereas overexpressing plants were drought tolerant, phenotypes reminiscent of myb96 mutant plants and MYB96-overexpressing plants. Taken together, these results demonstrate that LTP3 acts as a target of MYB96 to be involved in plant tolerance to freezing and drought stress.

In angiosperms, after the floral transition, the inflorescence meristem produces floral meristems (FMs). Determinate growth of FMs produces flowers of a particular size and form. This determinate growth requires specification of floral organs and termination of stem-cell divisions. Establishment of the FM and specification of outer whorl organs (sepals and petals) requires the floral homeotic gene APETALA1 (AP1). To determine FM identity, AP1 also prevents the formation of flowers in the axils of sepals. The mechanisms underlying AP1 function in the floral transition and in floral organ patterning have been studied extensively, but how AP1 terminates sepal axil stem-cell activities to suppress axillary secondary flower formation remains unclear. Here we show that AP1 regulates cytokinin levels by directly suppressing the cytokinin biosynthetic gene LONELY GUY1 and activating the cytokinin degradation gene CYTOKININ OXIDASE/DEHYDROGENASE3. Restoring the expression of these genes to wild-type levels in AP1-expressing cells or suppressing cytokinin signaling inhibits indeterminate inflorescence meristem activity caused by ap1 mutation. We conclude that suppression of cytokinin biosynthesis and activation of cytokinin degradation mediates AP1 function in establishing determinate FM. A deeper understanding of axil-lateral meristem activity provides crucial information for enhancing yield by engineering crops that produce more elaborated racemes.axillary meristem | indeterminacy

In flowering plants, the arrangement of flowers on a stem becomes an inflorescence, and a huge variety of inflorescence architecture occurs in nature. Inflorescence architecture also affects crop yield. In simple inflorescences, flowers form on a main stem; by contrast, in compound inflorescences, flowers form on branched stems and the branching pattern defines the architecture of the inflorescence. In this review, we highlight recent findings on the regulation of inflorescence architecture by cytokinin plant hormones. Results in rice (Oryza sativa) and Arabidopsis thaliana show that although these two species have distinct inflorescence architectures, cytokinins have a common effect on inflorescence branching. Based on these studies, we discuss how cytokinins regulate distinct types of inflorescence architecture through their effect on meristem activities.

Highlights d A self-activation loop maintains meristematic cells in the leaf axil d ATH1 is required for axillary meristem initiation d ATH1-STM heterodimer binds the STM locus to maintain its expression d Expression allows a permissive epigenetic environment at the STM locus

Plant responses to low temperature are tightly associated with defense responses. We previously characterized the chilling-sensitive mutant chs3-1 resulting from the activation of the Toll and interleukin 1 receptor-nucleotide binding-leucine-rich repeat (TIR-NB-LRR)-type resistance (R) protein harboring a C-terminal LIM (Lin-11, Isl-1 and Mec-3 domains) domain. Here we report the identification of a suppressor of chs3, ibr5-7 (indole-3-butyric acid response 5), which largely suppresses chilling-activated defense responses. IBR5 encodes a putative dual-specificity protein phosphatase. The accumulation of CHS3 protein at chilling temperatures is inhibited by the IBR5 mutation. Moreover, chs3-conferred defense phenotypes were synergistically suppressed by mutations in HSP90 and IBR5. Further analysis showed that IBR5, with holdase activity, physically associates with CHS3, HSP90 and SGT1b (Suppressor of the G2 allele of skp1) to form a complex that protects CHS3. In addition to the positive role of IBR5 in regulating CHS3, IBR5 is also involved in defense responses mediated by R genes, including SNC1 (Suppressor of npr1-1, Constitutive 1), RPS4 (Resistance to P. syringae 4) and RPM1 (Resistance to Pseudomonas syringae pv. maculicola 1). Thus, the results of the present study reveal a role for IBR5 in the regulation of multiple R protein-mediated defense responses.