SUMMARYReactive oxygen species (ROS) are produced in plant cells primarily as by-products of aerobic energy metabolism. They are also generated during plant adaptation responses to environmental stresses, such as drought and high salinity. Therefore, plants have evolved ROS-detoxifying enzymes and antioxidants to cope with ROS accumulation. However, if stress conditions are prolonged, the level of ROS will surpass the capacity of the detoxifying machinery, causing oxidative damage to cellular constituents. It is known that ROS act in abscisic acid-mediated stress responses to sustain plant survival under adverse growth conditions. However, it is largely unknown how ROS metabolism is linked to stress responses. Here, we show that a droughtresponsive NAC transcription factor NTL4 promotes ROS production by binding directly to the promoters of genes encoding ROS biosynthetic enzymes during drought-induced leaf senescence. Leaf senescence was accelerated in 35S:4DC transgenic plants over-expressing an active form of NTL4 under drought conditions. The 35S:4DC transgenic plants were hypersensitive to drought, and ROS accumulated in the leaves. In contrast, ROS levels were reduced in NTL4-deficient ntl4 mutants, which exhibited delayed leaf senescence and enhanced drought resistance. These observations indicate that NTL4 acts as a molecular switch that couples ROS metabolism to drought-induced leaf senescence in Arabidopsis.

Plants adjust their architecture to optimize growth and reproductive success under changing climates. Hypocotyl elongation is a pivotal morphogenic trait that is profoundly influenced by light and temperature conditions. While hypocotyl photomorphogenesis has been well characterized at the molecular level, molecular mechanisms underlying hypocotyl thermomorphogenesis remains elusive. Here, we demonstrate that the E3 ubiquitin ligase CONSTITUTIVE PHOTOMORPHOGENIC 1 (COP1) conveys warm temperature signals to hypocotyl thermomorphogenesis. To investigate the roles of COP1 and its target ELONGATED HYPOCOTYL 5 (HY5) during hypocotyl thermomorphogenesis, we employed Arabidopsis mutants that are defective in their genes. Transgenic plants overexpressing the genes were also produced. We examined hypocotyl growth and thermoresponsive turnover rate of HY5 protein at warm temperatures under both light and dark conditions. Elevated temperatures trigger the nuclear import of COP1, thereby alleviating the suppression of hypocotyl growth by HY5. While the thermal induction of hypocotyl growth is circadian-gated, the degradation of HY5 by COP1 is uncoupled from light responses and timing information. We propose that thermal activation of COP1 enables coincidence between warm temperature signaling and circadian rhythms, which allows plants to gate hypocotyl thermomorphogenesis at the most profitable time at warm temperatures.

Environmental sensitivity varies across developmental phases in flowering plants. In the juvenile phase, microRNA156 (miR156)-mediated repression of SQUAMOSA PROMOTER-BINDING PROTEIN-LIKE (SPL) transcription factors renders Arabidopsis plants incompetent to floral inductive signals, including long-day (LD) photoperiod. During the vegetative phase transition, which accompanies a reduction of miR156 and a concomitant elevation of its targets, plants acquire reproductive competence such that LD signals promote flowering. However, it remains largely unknown how developmental signals are associated with photoperiodic flowering. Here, we show that SPL3, SPL4, and SPL5 (SPL3/4/5) potentiate the FLOWERING LOCUS T (FT)-FD module in photoperiodic flowering. SPL3/4/5 function as transcriptional activators through the interaction with FD, a basic leucine zipper transcription factor which plays a critical role in photoperiodic flowering. SPL3/4/5 can directly bind to the promoters of APETALA1, LEAFY, and FRUITFULL, thus mediating their activation by the FT-FD complex. Our findings demonstrate that SPL3/4/5 act synergistically with the FT-FD module to induce flowering under LDs, providing a long-sought molecular knob that links developmental aging and photoperiodic flowering.

During cold acclimation, C-repeat binding factors (CBFs) activate downstream targets, such as cold-regulated genes, leading to the acquisition of freezing tolerance in plants. Inducer of CBF expression 1 (ICE1) plays a key role by activating CBF3 expression in shaping the cold-induced transcriptome. While the ICE1-CBF3 regulon constitutes a major cold acclimation pathway, gene regulatory networks governing the CBF signaling are poorly understood. Here, we demonstrated that ICE1 and its paralog ICE2 induce CBF1, CBF2, and CBF3 by binding to the gene promoters. ICE2, like ICE1, was ubiquitinated by the high expression of osmotically responsive gene 1 (HOS1) E3 ubiquitin ligase. Whereas ICE2-defective ice2-2 mutant did not exhibit any discernible freezing-sensitive phenotypes, ice1-2 ice2-2/+ plant, which is defective in ICE1 and has a heterozygotic ice2 mutation, exhibited significantly reduced freezing tolerance. Accordingly, all three CBF genes were markedly down-regulated in the ice1-2 ice2-2/+ plant, indicating that ICE1 and ICE2 are functionally redundant with different implementations in inducing CBF genes. Together with the negative regulation of CBF3 by CBF2, we propose that the unified ICE-CBF pathway provides a transcriptional feedback of freezing tolerance to sustain plant development and survival during cold acclimation.

Global warming is predicted to profoundly affect plant distribution and crop yield in the near future. Higher ambient temperature can influence diverse aspects of plant growth and development. In Arabidopsis, the basic helix-loop-helix transcription factor PHYTOCHROME-INTERACTING FACTOR 4 (PIF4) regulates temperature-induced adaptive responses by modulating auxin biosynthesis. At high temperature, PIF4 directly activates expression of YUCCA8 (YUC8), a gene encoding an auxin biosynthetic enzyme, resulting in auxin accumulation. Here we demonstrate that the RNA-binding protein FCA attenuates PIF4 activity by inducing its dissociation from the YUC8 promoter at high temperature. At 28°C, auxin content is elevated in FCA-deficient mutants that exhibit elongated stems but reduced in FCAoverexpressing plants that exhibit reduced stem growth. We propose that the FCA-mediated regulation of YUC8 expression tunes down PIF4-induced architectural changes to achieve thermal adaptation of stem growth at high ambient temperature.

Large vein allografts are suitable for middle hepatic vein (MHV) reconstruction, but their supply is often limited. Although polytetrafluoroethylene (PTFE) grafts are unlimitedly available, their long-term patency is relatively poor. We intended to enhance the clinical usability of PTFE grafts for MHV reconstruction during living donor liver transplantation (LDLT). Two sequential studies were performed. First, PTFE grafts were implanted as inferior vena cava replacements into dogs. Second, in a 1-year prospective clinical trial of 262 adults undergoing LDLT with a modified right lobe, MHV reconstruction with PTFE grafts was compared with other types of reconstruction, and the outcomes were evaluated. In the animal study, PTFE grafts induced strong inflammatory reactions and luminal thrombus formation, but the endothelial lining was well developed. In the clinical study, the reconstruction techniques were revised to make a composite PTFE graft with an artery patch on the basis of the results of the animal study. MHVs were reconstructed with cryopreserved iliac veins (n ¼ 122), iliac arteries (n ¼ 43), aortas (n ¼ 13), and PTFE (n ¼ 84), and these reconstructions yielded 6-month patency rates of 75.3%, 35.2%, 92.3%, and 76.6%, respectively. The overall 6-month patency rates for the iliac vein and PTFE grafts were similar (P ¼ 0.92), but the 6-month patency rates with vein segment 5 were 51.0% and 34.7%, respectively (P ¼ 0.001). The overall graft and patient survival rates did not differ among these 4 groups. In conclusion, ringed PTFE grafts combined with small vessel patches showed high patency rates comparable to those of iliac vein grafts; thus, they can be used for MHV reconstruction when other sizable vessel allografts are not available. Liver Transpl 18:955-965, 2012. V C 2012 AASLD.Received December 6, 2011; accepted March 19, 2012.Middle hepatic vein (MHV) reconstruction with an interposition vessel graft has been established as a standard procedure for living donor liver transplantation (LDLT) with a right lobe graft when the donor's MHV trunk is preserved in the donor's remnant liver.Materials used to date for this type of venous vascular reconstruction have included various types of homologous and autologous vessel grafts. [1][2][3][4][5] The recent increase in the number of adult LDLT procedures and the relatively limited number of vessel allografts have Abbreviations: CT, computed tomography; GRWR, graft-to-recipient weight ratio; IVC, inferior vena cava; LDLT, living donor liver transplantation; MELD, Model for End-Stage Liver Disease; MHV, middle hepatic vein; PTFE, polytetrafluoroethylene; V5, hepatic vein branch segment 5; V8, hepatic vein branch segment 8.

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