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Evolutionarily conserved DEK domain-containing proteins have been implicated in multiple chromatin-related processes, mRNA splicing and transcriptional regulation in eukaryotes. Here, we show that two DEK proteins, DEK3 and DEK4, control the floral transition in Arabidopsis. DEK3 and DEK4 directly associate with chromatin of related flowering repressors, FLOWERING LOCUS C (FLC), and its two homologs, MADS AFFECTING FLOWERING4 (MAF4) and MAF5, to promote their expression. The binding of DEK3 and DEK4 to a histone octamer in vivo affects histone modifications at FLC, MAF4 and MAF5 loci. In addition, DEK3 and DEK4 interact with RNA polymerase II and promote the association of RNA polymerase II with FLC, MAF4 and MAF5 chromatin to promote their expression. Our results show that DEK3 and DEK4 directly interact with chromatin to facilitate the transcription of key flowering repressors and thus prevent precocious flowering in Arabidopsis.Flavonoids with great medicinal value play an important role in plant individual growth and stress resistance. Flavonol synthetase (FLS) is one of the key enzymes to synthesize flavonoids. However, the role of the FLS gene in flavonoid accumulation and tolerance to abiotic stresses, as well as its mechanism has not yet been investigated systematically in plants. The aim of this research is to evaluate the effect of FLS overexpression on the accumulation of active ingredients and stress resistance in Euphorbia kansui Liou. The results showed that when the EkFLS gene was overexpressed in Arabidopsis thaliana, the accumulation of flavonoids was improved. In addition, when the wild-type and EkFLS overexpressed Arabidopsis plants were treated with ABA and MeJA, compared with WT Arabidopsis, EkFLS overexpressed Arabidopsis promoted stomatal aperture to influence photosynthesis of the plants, which in turn can promote stress resistance. Meanwhile, under MeJA, NaCl, and PEG treatment, EkFLS overexpressed in Arabidopsis induced higher accumulation of flavonoids, which significantly enhanced peroxidase (POD) and superoxide dismutase (SOD) activities that can scavenge reactive oxygen species in cells to protect the plant. These results indicated that EkFLS overexpression is strongly correlated to the increase of flavonoid synthesis and therefore the tolerance to abiotic stresses in plants, providing a theoretical basis for further improving the quality of medicinal plants and their resistance to abiotic stresses simultaneously.Plant virus movement proteins (MPs) facilitate virus spread in their plant hosts, and some of them are known to target plasmodesmata (PD). However, how the MPs target PD is still largely unknown. Carrot mottle virus (CMoV) encodes the ORF3 and ORF4 proteins, which are involved in CMoV movement. In this study, we used CMoV as a model to study the PD targeting of a plant virus MP. We showed that the CMoV ORF4 protein, but not the ORF3 protein, modified PD and led to the virus movement. We found that the CMoV ORF4 protein interacts with the host cell small ubiquitin-like modifier (SUMO) 1, 2 and the SUMO-conjugating enzyme SCE1, resulting in the ORF4 protein SUMOylation. CA-074 Me nmr Downregulation of mRNAs for NbSCE1 and NbSUMO impaired CMoV infection. The SUMO-interacting motifs (SIMs) LVIVF, VIWV, and a lysine residue at position 78 (K78) are required for the ORF4 protein SUMOylation. The mutation of these motifs prevented the protein to efficiently target PD, and further slowed or completely abolished CMoV systemic movement. Finally, we found that some of these motifs are highly conserved among umbraviruses. Our data suggest that the CMoV ORF4 protein targets PD by interacting with the host cell SUMOylation system.Previously, dibutyltin dichloride (DBTC) was the putative toxophore for dibutyltin bis-alkyl and bis-thio esters. Recent chemical and toxicological data on dioctyltin bis(2-ethylhexyl thioglycolate) suggest the thioglycolate esters of alkyltins do not generate the dichloride toxophore. Our results, using 119 Sn-nuclear magnetic resonance (NMR) spectroscopy, demonstrated that dibutyltin bis(2-ethylhexyl thioglycolate) (DBTE) is hydrolyzed to dibutyltin chloro-(2-ethylhexyl thioglycolate) (DBTEC) under simulated gastric conditions. No DBTC was detected. DBTE was administered orally to presumed-pregnant Sprague-Dawley rats in a corn oil vehicle at 2.5, 8.5, and 25.0 mg/kg/day (Gestation Day 5 [GD5] through GD19). There were no maternal deaths, no treatment-related statistically significant reductions in feed consumption, maternal body weight or weight gain, or adverse gestational outcomes. Maternal thymus weight was significantly reduced in rats at 25 mg/kg. There were no effects on fetal growth, no dose-dependent pattern of external, visceral, or skeletal malformations, and no increase in anatomical variations. Based on the obtained experimental data, it is concluded here that DBTE forms DBTEC, not DBTC, in the stomach, and DBTE was not teratogenic nor fetotoxic in rats, a species sensitive to DBTC. The maternal no-observed-adverse-effect level (NOAEL) was 8.5 mg/kg/day, and the developmental NOAEL was 25 mg/kg/day, the high dose. The maternal LOAEL was 25 mg/kg/day based on reduced maternal thymus weight.
To determine the pixel sensitivity map (PSM) for amorphous silicon electronic portal imaging devices (EPIDs) using a single flood field signal.

A raw EPID signal results from the incident particle energy fluence, the inherent pixels response, and the background signal. In large open fields, particle energy fluence is a slow-varying signal that is locally considered spatially constant. Pixels response is a fast and abrupt varying behavior. The background signal is due to the EPID panel electronics, which is determined during radiation absence. To determine the PSM, after correcting for the background signal, we apply a model that captures the underlying smooth particle energy fluence-induced signal. This fluence signal-fitted model is then used to determine the PSM. Here, we use a polynomial-based regression surface model in both x and y dimensions. To validate the generated PSM, we measure beams and compute PSMs for multiple beam energies with and without flattening filters and for multiple source-to-imager distances.
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