Physiological Characteristic Changes and Transcriptome Analysis of Maize (Zea mays L.) Roots under Drought Stress.

Water deficit is a key limiting factor for limiting yield in maize (Zea mays L.). It is crucial to elucidate the molecular regulatory networks of stress tolerance for genetic enhancement of drought tolerance. The mechanism of drought tolerance of maize was explored by comparing physiological and transcriptomic data under normal conditions and drought treatment at polyethylene glycol- (PEG-) induced drought stress (5%, 10%, 15%, and 20%) in the root during the seedling stage. The content of saccharide, SOD, CAT, and MDA showed an upward trend, proteins showed a downward trend, and the levels of POD first showed an upward trend and then decreased. Compared with the control group, a total of 597, 2748, 6588, and 5410 differentially expressed genes were found at 5%, 10%, 15%, and 20% PEG, respectively, and 354 common DEGs were identified in these comparisons. Some differentially expressed genes were remarkably enriched in the MAPK signaling pathway and plant hormone signal transduction. The 50 transcription factors (TFs) divided into 15 categories were screened from the 354 common DEGs during drought stress. Auxin response factor 10 (ARF10), auxin-responsive protein IAA9 (IAA9), auxin response factor 14 (ARF14), auxin-responsive protein IAA1 (IAA1), auxin-responsive protein IAA27 (IAA27), and 1 ethylene response sensor 2 (ERS2) were upregulated. The two TFs, including bHLH 35 and bHLH 96, involved in the MAPK signal pathway and plant hormones pathway, are significantly upregulated in 5%, 10%, 15%, and 20% PEG stress groups. The present study provides greater insight into the fundamental transcriptome reprogramming of grain crops under drought.

CTRP3 attenuates inflammation, oxidative and cell death in cisplatin induced HK-2 cells.

Cisplatin has been widely studied and found to be a highly effective anti-tumor drug. It has several side effects, including acute kidney injury (AKI). Cisplatin-induced AKI can be primarily attributed to oxidative stress, inflammation, and apoptosis. The CTRP3 adipokine is a new adipokine that exhibits antioxidant, anti-inflammatory, and antiapoptotic properties. Despite this, the role of CTRP3 in AKI remain unclear. In cisplatin-induced AKI models, our findings demonstrated that CTRP3 expression was decreased in human proximal tubule epithelial cells (HK-2). In the in vitro experiments, HK-2 cells were first transfected with an overexpression plasmid of CTRP3 (pcDNA-CTRP3) or a small interfering RNA for CTRP3 (si-CTRP3) and induced by cisplatin; and cell oxidative stress, inflammation, proliferation, and apoptosis were found to be present. Overexpressing CTRP3 inhibited oxidative stress through decreasing malondialdehyde (MDA) levels and increasing the activity of SOD and CAT. The mRNA levels of SOD1 and SOD2 were increased in response to CTRP3 overexpression. Additionally, CTRP3 decreased TNF-α and MCP-1 levels. Moreover, CTRP3 overexpression increased cisplatin-induced cell activity and decreased cell apoptosis, as indicated by the elevated numbers of EdU positive cells and decreased numbers of apoptotic cells. Consistent with these results, the overexpression of CTRP3 effectively elevated the mRNA levels of Bcl-2 and reduced the mRNA levels of Bax. In contrast, inhibition of CTRP3 expression by si-CTRP3 reversed the cisplatin-induced indices. Mechanistically, we found that the overexpression of CTRP3 can increase expression of Nrf2 and inhibit the activation of MAPK phosphorylation (ERK, JNK, and p38). Furthermore, inhibition of ERK, JNK and p38 activity eliminated aggravation of cisplatin-induced inflammation and apoptosis caused by CTRP3 knockdown. Additionally, the cisplatin-induced oxidative stress and activation of MAPK phosphorylation (ERK, JNK, and p38) in HK-2 cells were reversed by Nrf2 suppression by siRNA. Collectively, these results indicated that CTRP3 may identify as a novel target for AKI treatment and protect against cisplatin-induced AKI through the Nrf2/MAPK pathway.

SNP-based bulk segregant analysis revealed disease resistance QTLs associated with northern corn leaf blight in maize.

Maize (Zea mays L.) is the most important food security crop worldwide. Northern corn leaf blight (NCLB), caused by Exserohilum turcicum, severely reduces production causing millions of dollars in losses worldwide. Therefore, this study aimed to identify significant QTLs associated with NCLB by utilizing next-generation sequencing-based bulked-segregant analysis (BSA). Parental lines GML71 (resistant) and Gui A10341 (susceptible) were used to develop segregating population F2. Two bulks with 30 plants each were further selected from the segregating population for sequencing along with the parental lines. High throughput sequencing data was used for BSA. We identified 10 QTLs on Chr 1, Chr 2, Chr 3, and Chr 5 with 265 non-synonymous SNPs. Moreover, based on annotation information, we identified 27 candidate genes in the QTL regions. The candidate genes associated with disease resistance include AATP1, At4g24790, STICHEL-like 2, BI O 3-BIO1, ZAR1, SECA2, ABCG25, LECRK54, MKK7, MKK9, RLK902, and DEAD-box ATP-dependent RNA helicase. The annotation information suggested their involvement in disease resistance-related pathways, including protein phosphorylation, cytoplasmic vesicle, protein serine/threonine kinase activity, and ATP binding pathways. Our study provides a substantial addition to the available information regarding QTLs associated with NCLB, and further functional verification of identified candidate genes can broaden the scope of understanding the NCLB resistance mechanism in maize.

Vanillin attenuates the ethanol withdrawal syndrome and ethanol withdrawal induced anxiety by regulating the neurochemical balance.

Ethanol abuse is a major public issue globally and withdrawal of ethanol after chronic exposure contributes to the development of behavioural changes. The present study evaluates vanillin effect against the ethanol withdrawal syndrome (EWS) and the associated anxiety. Rats were exposed to ethanol for 21 days at 7.2% concentration maximum with drinking water in a modified liquid diet. Vanillin at doses of 100 and 200 mg/kg were administered 30 min prior to ethanol withdrawal, and behavioural changes were observed at 1st, 2nd, 4th, 6th and 12th h of ethanol withdrawal. Moreover, the locomotor activity was assessed using the astrophotometer and level of anxiety by the elevated plus maze. The level of neurotransmitters and mRNA expression of corticotropin-releasing factor (CRF) and corticotropin releasing factor receptor 1 (CRFR1) were estimated in brain tissue of vanillin treated EWS rats. There was a significant improvement in the ethanol withdrawal behaviour in the vanillin treated group compared to EWS rats. The locomotor activity and level of anxiety was observed to be reduced significantly (p < 0.01) in the vanillin treated group compared to EWS rats. Treatment with vanillin ameliorates the altered level of g-aminobutyric acid (GABA), dopamine and glutamate and level of corticosterone in ethanol withdrawal rats. mRNA expression of CRF and CRFR1 was reduced significantly (p < 0.01) in brain tissue of the vanillin treated group compared to the EWS group of rats. In conclusion, data reveal that treatment with vanillin shows a beneficial effect against EWS and ethanol withdrawal associated anxiety by regulating CRF/CRFR1 expression.