During plant development, because no cell movement takes place, control of the timing and extent of cell division and coordination of the direction and extent of cell expansion are particularly important for growth and development. The plant hormone gibberellins (GAs) play key roles in the control of these developmental processes. However, little is known about the molecular components that integrate the generic GA signaling into a specific cell/tissue to coordinate cell division and cell expansion. Here we report that SCARECROW-LIKE 3 (SCL3), a GRAS protein, acts as a positive regulator to integrate and maintain a functional GA pathway by attenuating the DELLA repressors in the root endodermis. The tissue-specific maintenance of GA signaling in the root endodermis plays distinct roles along the longitudinal root axis. While in the elongation/differentiation zone (EDZ), the endodermis-confined GA pathway by SCL3 controls primarily coordination of root cell elongation; in the meristem zone (MZ) SCL3 in conjunction with the SHORT-ROOT/SCARECROW (SHR/SCR) pathway controls GA-modulated ground tissue maturation. Our findings highlight the regulatory network of the GRAS transcription regulators (SCL3, DELLAs, and SHR/SCR) in the root endodermis, shedding light on how GA homeostasis is achieved and how the maintenance of GA signaling controls developmental processes in roots.

Cold induces expression of a number of genes that encode proteins that enhance tolerance to freezing temperatures in plants 1,2 . A cis-acting element responsive to cold and drought, the C-repeat/dehydration-responsive element (C/DRE), was identified in the Arabidopsis thaliana stress-inducible genes

GRAS proteins belong to a plant-specific transcription factor family. Currently, 33 GRAS members including a putative expressed pseudogene have been identified in the Arabidopsis genome. With a reverse genetic approach, we have constructed a ''phenome-ready unimutant collection'' of the GRAS genes in Arabidopsis thaliana. Of this collection, we focused on loss-of-function mutations in 23 novel GRAS members. Under standard conditions, homozygous mutants have no obvious morphological phenotypes compared with those of wild-type plants. Expression analysis of GRAS genes using quantitative realtime RT-PCR (qRT-PCR), microarray data mining, and promoter::GUS reporter fusions revealed their tissuespecific expression patterns. Our analysis of protein-protein interaction and subcellular localization of individual GRAS members indicated their roles as transcription regulators. In our yeast two-hybrid (Y2H) assay, we confirmed the protein-protein interaction between SHORT-ROOT (SHR) and SCARECROW (SCR). Furthermore, we identified a new SHR-interacting protein, SCARECROW-LIKE23 (SCL23), which is the most closely related to SCR. Our large-scale analysis provides a comprehensive evaluation on the Arabidopsis GRAS members, and also our phenome-ready unimutant collection will be a useful resource to better understand individual GRAS proteins that play diverse roles in plant growth and development.

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Objective. MicroRNAs (miRNAs), small noncoding RNA molecules, are involved in the pathogenesis of various diseases such as cancer and arthritis. The aim of this study was to determine whether miR-127-5p regulates interleukin-1␤ (IL-1␤)-induced expression of matrix metalloproteinase 13 (MMP-13) and other catabolic factors in human chondrocytes.Methods. Expression of miR-127-5p and MMP-13 by normal and osteoarthritic (OA) human cartilage was determined using real-time polymerase chain reaction. The effect of miR-127-5p on MMP-13 expression was evaluated using transient transfection of human chondrocytes or chondrogenic SW-1353 cells with miR-127-5p or its antisense inhibitor (anti-miR-127-5p). MMP-13 protein production was quantified by enzymelinked immunosorbent assay, and the involvement of miR-127-5p in IL-1␤-mediated catabolic effects was examined by immunoblotting. MicroRNA-127-5p binding with the putative site in the 3 -untranslated region (3 -UTR) of MMP-13 messenger RNA (mRNA) was validated by luciferase reporter assay.Results. There was a significant reduction in miR-127-5p expression in OA cartilage compared with normal cartilage. Up-regulation of MMP-13 expression by IL-1␤ was correlated with down-regulation of miR-127-5p expression in human chondrocytes. MicroRNA-127-5p suppressed IL-1␤-induced MMP-13 production as well as the activity of a reporter construct containing the 3 -UTR of human MMP-13 mRNA. In addition, mutation of the miR-127-5p binding site in the 3 -UTR of MMP-13 mRNA abolished miR-127-5p-mediated repression of reporter activity. Conversely, treatment with anti-miR-127-5p remarkably increased reporter activity and MMP-13 production. Interestingly, the IL-1␤-induced activation of JNK, p38, and NF-B and expression of MMP-1 and cyclooxygenase 2 were significantly inhibited by miR-127-5p. Conclusion. MicroRNA-127-5p is an important regulator of MMP-13 in human chondrocytes and may contribute to the development of OA.Osteoarthritis (OA) is a degenerative disease of articular cartilage characterized by loss of the cartilage matrix, mainly collagen and proteoglycans, leading to tissue destruction and loss of joint function. Although OA is regarded as a noninflammatory form of arthritis, considerable evidence suggests that proinflammatory cytokines derived from the synovium and chondrocytes play a role in cartilage destruction. The activity of the proinflammatory cytokine interleukin-1␤ (IL-1␤) and its downstream mediators leads to up-regulation of matrix metalloproteinase (MMP) and a decrease in the synthesis of the cartilage extracellular matrix (ECM) (1). Among the target mediators of IL-1␤, MMP-13 has gained the most interest, due to its capacity to degrade collagens along with a wide range of matrix molecules (2).A variety of therapeutic strategies for OA have thus been developed to antagonize the activity of MMP-13; however, the toxicity of nonspecific MMP inhibitors has hampered their application in clinical settings. A detailed analysis of the mechanism of regulation of MMP-13 in chondro...