SummaryThe HUA2 gene acts as a repressor of floral transition. Lesions in hua2 were identified through a study of natural variation and through two mutant screens. An allele of HUA2 from Landsberg erecta (Ler) contains a premature stop codon and acts as an enhancer of early flowering 4 (elf4) mutants. hua2 single mutants, in the absence of the elf4 lesion, flower earlier than wild type under short days. hua2 mutations partially suppress late flowering in FRIGIDA (FRI )-containing lines, autonomous pathway mutants, and a photoperiod pathway mutant. hua2 mutations suppress late flowering by reducing the expression of several MADS genes that act as floral repressors including FLOWERING LOCUS C (FLC ) and FLOWERING LOCUS M (FLM ).

SummaryCREB-binding protein (CBP) and its homolog p300 possess histone acetyltransferase activity and function as key transcriptional co-activators in the regulation of gene expression that controls differentiation and development in animals. However, the role of CBP/p300-like genes in plants has not yet been elucidated. Here, we show that Arabidopsis CBP/p300-like genes promote flowering by affecting the expression of a major floral repressor FLOWERING LOCUS C (FLC). Although animal CBP and p300 generally function as co-activators, Arabidopsis CBP/p300-like proteins are required for the negative regulation of FLC. This CBP/p300-mediated FLC repression may involve reversible protein acetylation independent of histone modification within FLC chromatin.

SUPPRESSOR OF OVEREXPRESSION OF CO1 (SOC1) is regulated by a complex transcriptional regulatory network that allows for the integration of multiple floral regulatory inputs from photoperiods, gibberellin, and FLOWERING LOCUS C. However, the posttranscriptional regulation of SOC1 has not been explored. Here, we report that EARLY FLOWERING9 (ELF9), an Arabidopsis thaliana RNA binding protein, directly targets the SOC1 transcript and reduces SOC1 mRNA levels, possibly through a nonsense-mediated mRNA decay (NMD) mechanism, which leads to the degradation of abnormal transcripts with premature translation termination codons (PTCs). The fully spliced SOC1 transcript is upregulated in elf9 mutants as well as in mutants of NMD core components. Furthermore, a partially spliced SOC1 transcript containing a PTC is upregulated more significantly than the fully spliced transcript in elf9 in an ecotype-dependent manner. A Myc-tagged ELF9 protein (MycELF9) directly binds to the partially spliced SOC1 transcript. Previously known NMD target transcripts of Arabidopsis are also upregulated in elf9 and recognized directly by MycELF9. SOC1 transcript levels are also increased by the inhibition of translational activity of the ribosome. Thus, the SOC1 transcript is one of the direct targets of ELF9, which appears to be involved in NMD-dependent mRNA quality control in Arabidopsis.

Diallyl disulfide (DADS) is the most prevalent oil-soluble sulfur compound in garlic and inhibits cell proliferation in many cancer cell lines. Here we examined DADS cytotoxicity in a redox-mediated process, involving reactive oxygen species (ROS) production. In the present study, p53-independent cell cycle arrest at G2/M phase was observed with DADS treatment, along with time-dependent increase of cyclin B1. In addition, apoptosis was also observed upon 24-h DADS treatment accompanied by activation of p53. In HCT-116 cells, DADS application induced a dose-dependent increase and time-dependent changes in ROS production. Scavenging of DADS-induced ROS by N-acetyl cysteine or reduced glutathione inhibited cell cycle arrest, apoptosis and p53 activation by DADS. These results suggest that ROS trigger the DADS-induced cell cycle arrest and apoptosis and that ROS are involved in stress-induced signaling upstream of p53 activation. Transfection of p53 small interfering RNA prevents the accumulation of cleaved poly(ADP-ribose) polymerase and sub-G1 cell population by 65% and 35%, respectively. Moreover, DADS-induced apoptosis was also prevented by treatment with oligomycin, which is known to prevent p53-dependent apoptosis by reducing ROS levels in mitochondria. These results suggest that mitochondrial ROS may serve as second messengers in DADS-induced apoptosis, which requires activation of p53.

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We investigated the differential expression of seven ACC synthase and two ACC oxidase genes in mun8 bean leaves. Among these, only.4C~2, .4C01, and ACO2 were expressed in etiolated leaves. When seedlings were de-etiolated, the expression level of ACO/ decreased by 65%, expression of AC02 disappeared, while that of ACS2 was unchanged. For de-etiolated leaves treated with NaCI in the dark, the photochemical efficiency of PSII was not altered, and no genes were newly induced within the first 12 h. However, in the presence of light, transcripts of ACSI, AC~3, AC~4, and ACS6 were newly accumulated, and the expression levels of ACS2 and ACO/were increased. The kinetics of transcript accumulation in response to methyl viologen (MV) treatment in the light were similar to those observed in the NaCI-treated leaves in the presence of light, suggesting that changes in the latter were caused by oxidative, rather than saline, stress. However, transcripts from most of the genes began accumulating more slowly in MV-treated leaves, with those of ACS1 and AC~6 accumulating in much lower amounts than in NaCI-treated leaves. The reverse was true for AC54 transcripts.

The work of the fuel engine is based on the fuel entering and expelling high-pressure tubing. The intermittent work of the fuel entering and expelling will lead to the change of pressure in the high-pressure tubing. This paper established the time control model to carry out the research. For the first question, we made the fuel entry period and injection period equal to 100ms. Because of Δ P Δ ρ = E ρ , the volume of the high-pressure tubing remained constant, and the fuel mass into the high-pressure tubing was equal to the fuel mass ejected from the high-pressure tubing. The density time control model was established under the condition of mass conservation, and the opening time of each time was obtained to be 0.275ms. For the second question, we set the pressure increase after each fuel entry in the adjustment process to be equal. Due to Δ P Δ ρ = E ρ , we obtained the new density value of the high-pressure tubing, and substituted the density and time model to obtain the opening time of each one-way valve.

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