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WRKY proteins play crucial roles in various plant processes. An AtWRKY12 homologous gene, named MlWRKY12, was isolated from Miscanthus lutarioriparius. The MlWRKY12 gene encodes a WRKY transcription factor belonging to the group IIc subfamily. MlWRKY12 is a nuclear protein. Gene expression pattern analysis revealed a relatively high MlWRKY12 expression level in rhizomes, stems and leaf sheaths. In situ hybridization analysis further demonstrated that MlWRKY12 was expressed in vascular bundle sheath, sclerenchyma and parenchyma tissues. The heterologous expression of MlWRKY12 in an atwrky12 background mutant successfully rescued the phenotype of pith cell walls caused by the defect of AtWRKY12. Most strikingly, the transgenic Arabidopsis plants overexpressing MlWRKY12 exhibited early flowering. The transcript abundance of flowering related genes was measured by quantitative RT-PCR analysis, suggesting that overexpression of MlWRKY12 in Arabidopsis had a significant impact on the expression level of CONSTANS (CO). Moreover, the expression levels of FLOWERING LOCUS T (FT), LFY (LEAFY), APETALA1 (AP1), CAULIFLOWER (CAL) and FRUITFULL (FUL) were upregulated in transgenic plants. These results demonstrated the conserved function of MlWRKY12 existing in secondary cell wall formation of monocotyledonous species and implied a possible impact of MlWRKY12 on flowering control., (Copyright © 2013 Elsevier Ireland Ltd. All rights reserved.)

Circadian clocks generate endogenous rhythms in most organisms from cyanobacteria to humans and facilitate entrainment to environmental diurnal cycles, thus conferring a fitness advantage. Both transcriptional and posttranslational mechanisms are prominent in the basic network architecture of circadian systems. Posttranscriptional regulation, including mRNA processing, is emerging as a critical step for clock function. However, little is known about the molecular mechanisms linking RNA metabolism to the circadian clock network. Here, we report that a conserved SNW/Ski-interacting protein (SKIP) domain protein, SKIP, a splicing factor and component of the spliceosome, is involved in posttranscriptional regulation of circadian clock genes in Arabidopsis thaliana. Mutation in SKIP lengthens the circadian period in a temperature-sensitive manner and affects light input and the sensitivity of the clock to light resetting. SKIP physically interacts with the spliceosomal splicing factor Ser/Arg-rich protein45 and associates with the pre-mRNA of clock genes, such as PSEUDORESPONSE REGULATOR7 (PRR7) and PRR9, and is necessary for the regulation of their alternative splicing and mRNA maturation. Genome-wide investigations reveal that SKIP functions in regulating alternative splicing of many genes, presumably through modulating recognition or cleavage of 5' and 3' splice donor and acceptor sites. Our study addresses a fundamental question on how the mRNA splicing machinery contributes to circadian clock function at a posttranscriptional level.

Nuclear Factor I (Nfi) genes encode transcription factors essential for the development of organ systems including the lung. Nfib null mice die at birth with immature lungs. Nfib hemizygous mice have reduced lung maturation with decreased survival. We therefore hypothesized that these mice would be more sensitive to lung injury and would have lower survival to hyperoxia. Adult Nfib hemizygous mice and their wild-type (Wt) littermates were exposed to 100% O2 for 89, 80, 72 and 66 h for survival studies with lung outcome measurements at 66 h. Nfib hemizygous and Wt controls were also studied in RA at 66 h. Cell counts and cytokines were measured in bronchoalveolar lavage (BAL); lung sections examined by histopathology; lung angiogenic and oxidative stress gene expression assessed by real-time PCR. Unexpectedly, Nfib hemizygous mice (0/14-0%) had significantly lower mortality compared to Wt mice (10/22-45%) at 80 h of hyperoxia (P < 0.003). LD50 was 80 h in the Wt group versus 89 h in the hemizygous group. There were no differences in BAL cell counts between the groups. Among the cytokines studied, MIP-2 was significantly lower in hemizygous mice exposed to hyperoxia. New vessel formation, edema, congestion, and alveolar hemorrhage were noted on histopathology at 72 and 80 h in wild-type mice. Nfib hemizygous lungs had significant downregulation of genes involved in redox signaling and inflammatory pathways. Adult Nfib hemizygous mice are relatively resistant to hyperoxia compared to wild-type littermates. Mechanisms contributing to this resistance are not clear; however, transcription factors such as Nfib may regulate cell survival and play a role in modulating postnatal lung development. [ABSTRACT FROM AUTHOR]