Search

Zinc finger proteins (ZFPs) are transcription factors involved in multiple cellular functions. We identified a C2H2 type ZFP (MtZPT2-2) in Medicago truncatula and demonstrated that it localizes to the nucleus and inhibits the transcription of 2 genes encoding high-affinity potassium transporters (MtHKT1;1 and MtHKT1;2). MtZPT2-2 transcripts were detected in stem, leaf, flower, seeds and roots, with the highest level in the xylem and phloem of roots and stems. MtZPT2-2 transcription in leaves was reduced after salt stress. Compared with the wild-type (WT), transgenic lines overexpressing MtZPT2-2 had decreased salt tolerance, while MtZPT2-2–knockout mutants showed increased salt tolerance. MtHKT1;1 and MtHKT1;2 transcripts and Na+ accumulation in shoots and roots, as well as in the xylem of all genotypes of plants, were increased after salt treatment, with higher levels of MtHKT1;1 and MtHKT1;2 transcripts and Na+ accumulation in MtZPT2-2–knockout mutants and lower levels in MtZPT2-2–overexpressing lines compared with the WT. K+ levels showed no significant difference among plant genotypes under salt stress. Moreover, MtZPT2-2 was demonstrated to bind with the promoter of MtHKT1;1 and MtHKT1;2 to inhibit their expression. Antioxidant enzyme activities and the gene transcript levels were accordingly upregulated in response to salt, with higher levels in MtZPT2-2–knockout mutants and lower levels in MtZPT2-2–overexpressing lines compared with WT. The results suggest that MtZPT2-2 regulates salt tolerance negatively through downregulating MtHKT1;1 and MtHKT1;2 expression directly to reduce Na+ unloading from the xylem and regulates antioxidant defense indirectly. A zinc finger transcription factor negatively regulates salt tolerance by repressing the expression of genes encoding high-affinity potassium transporters. [ABSTRACT FROM AUTHOR]

Nonnegative matrix factorization (NMF) and its numerous variants have been extensively studied and used in hyperspectral unmixing (HU). With the aid of the designed deep structure, deep NMF-based methods demonstrate advantages in exploring the hierarchical features of complex data. However, a noise corruption problem commonly exists in hyperspectral data and severely degrades the unmixing performance of deep NMF-based methods when applied to HU. In this study, we propose an ℓ 2 , 1 norm-based robust deep nonnegative matrix factorization ( ℓ 2 , 1 -RDNMF) for HU, which incorporates an ℓ 2 , 1 norm into the two stages of the deep structure to achieve robustness. The multiplicative updating rules of ℓ 2 , 1 -RDNMF are efficiently learned and provided. The efficiency of the presented method is verified in experiments using both synthetic and genuine data. [ABSTRACT FROM AUTHOR]

The noise corruption problem commonly exists in hyperspectral images (HSIs) and severely affects the accuracy of hyperspectral unmixing algorithms. The noise formulation existing in HSIs is relatively complex and would change in conjunction with different devices and imaging settings. For real applications, applying denoising approaches without accurate close-to-reality noise modeling before unmixing may not improve, but rather degrade the unmixing performance. This study proposes a robust hyperspectral unmixing method with practical learning-based hyperspectral image denoising. We formulated a close-to-reality noise model for hyperspectral data and provide a calibration approach for the noise parameters. On the basis of the calibrated noise model, synthetic data were generated and used for training a KST-based denoising network. The noisy hyperspectral data were firstly denoised by the trained denoising network and were then used to perform the unmixing process. A variety of unmixing algorithms can be integrated into our method to improve the accuracy of unmixing in noisy situations. In the experiments, several widely used unmixing algorithms were employed to verify the effect of the proposed method. The experimental results on both synthetic and real demonstrated that our proposed method can handle HSI data with various gain settings and helps to improve the unmixing performance effectively. [ABSTRACT FROM AUTHOR]

HAK/KUP/KT transporters play an important role in maintaining K+ and Na+ homeostasis in plants in response to salt stress. A salt induced PvHAK16 from halophyte seashore paspalum (Paspalum vaginatum O. Swartz) was identified in this study. PvHAK16 was localized in the plasma membrane and highly expressed in leaves but not in roots. Overexpression of PvHAK16 in Arabidopsis led to reduced seed germination rate, shoot weight, F v / F m and survival rate but increased ion leakage after salt stress as compared with the wild type. Increased Na+ and decreased K+ levels that led to higher Na+/K+ ratio was observed in transgenic lines after salt stress, which was a result of the net influx of Na+ and net efflux of K+ in transgenic plants. The results suggest that PvHAK16 confers Na+ uptake and K+ efflux under salt stress and thus negatively regulates salt tolerance. Moreover, PvHAK16 expression altered transcript levels of ion homeostasis genes K + -Uptake Permease 7 (KUP7), Potassium Transport 2/3 (AKT2), Salt Overly Sensitive 1 (SOS1) and Gated Outwardly-Rectifying K + Channel (GORK), which were associated with the increased Na+/K+ ratio in transgenic plants. Transgenic plants had reduced transcript levels of stress responsive genes and showed promoted oxidative damage as a result of reduced SOD activity and proline accumulation. • PvHAK16 negatively regulates salt tolerance with increased Na+/K+ ratio. • PvHAK16 confers Na+ uptake and K+ efflux under salt stress. • PvHAK16 expression leads to reduced proline accumulation under salt stress. [ABSTRACT FROM AUTHOR]

Background: Lymph node metastasis is a poor prognostic factor for lung cancer. However, the risk of lymph node metastasis has not yet been clarified. This study was conducted to analyze the predictive factors for lymph node metastasis in patients with clinical-stage IA3 lung adenocarcinoma. Methods: We retrospectively analyzed all surgical patients with clinical stage IA3 lung adenocarcinoma admitted to our hospital from January 2017 to January 2022. Three hundred and thirty-four patients underwent lobectomy combined with systematic lymph node dissection. Univariate and multivariate logistic regression analyses were used to predict the risk factors of lymph node metastasis. Results: Of the 334 patients eligible for this study, the overall lymph node metastasis rate was 15.3%. There were 45 cases with N1 metastasis, 11 cases with N2 metastasis, and five cases with both N1 and N2 metastasis. The lymph node metastasis rate was 18.1% in patients with a consolidation tumor ratio (CTR) of >0.75, 57.9% in those with >5 ng/mL carcinoembryonic antigen (CEA), and 18.0% in those with a maximum standardized uptake value of >5. Receiver operating characteristic (ROC) curve analysis showed that the area under the curve (AUC) for CTR and CEA was 0.790 [95% confidence interval (CI): 0.727–0.853, P < 0.001] and 0.682 (95% CI: 0.591–0.773, P < 0.001), respectively. According to multivariate regression analysis, CEA (>5 ng/mL) [odds ratio (OR) = 3.05, P = 0.016] and CTR (>0.75) (OR = 2.75, P = 0.025) were significantly correlated with lymph node metastasis of clinical stage IA3 lung adenocarcinoma. Conclusions: CEA (>5 ng/mL) and CTR (>0.75) are two important predictors of lymph node metastasis in patients with clinical stage IA3 lung adenocarcinoma. [ABSTRACT FROM AUTHOR]

Summary: Leucine‐rich repeat‐receptor‐like kinase (LRR‐RLK) is a large subfamily of plant RLKs; however, its role in cold tolerance is still unknown. A novel cold tolerance LRR‐RLK gene (MtCTLK1) in Medicago truncatula was identified using the transgenic lines overexpressing MtCTLK1 (MtCTLK1‐OE) and mtctlk1 lines with Tnt1 retrotransposon insertion. Compared with the wild‐type, MtCTLK1‐OE lines had increased cold tolerance and mtctlk1 showed decreased cold tolerance. The impaired cold tolerance in mtctlk1 could be complemented by the transgenic expression of MtCTLK1 or its homolog MfCTLK1 from Medicago falcata. Antioxidant enzyme activities and proline accumulation as well as transcript levels of the associated genes were increased in response to cold, with higher levels in MtCTLK1‐OE or lower levels in mtctlk1 lines as compared with wild type. C‐Repeat‐Binding Factors (CBFs) and CBF‐dependent cold‐responsive genes were also induced in response to cold, and higher transcript levels of CBFs and CBF‐dependent cold‐responsive genes were observed in MtCTLK1‐OE lines whereas lower levels in mtctlk1 mutants. The results validate the role of MtCTLK1 or MfCTLK1 in the regulation of cold tolerance through the CBF pathway, antioxidant defense system and proline accumulation. It also provides a valuable gene for the molecular breeding program to improve cold tolerance in crops. Significance Statement: A novel cold tolerance leucine‐rich repeat‐receptor‐like kinase was identified from Medicago truncatula. It confers cold tolerance through regulation on the C‐repeat‐binding factor cold response pathway, antioxidant defense, and proline accumulation. [ABSTRACT FROM AUTHOR]

Loss of ARID1A, a subunit of the SWI/SNF chromatin remodeling complex, contributes to malignant progression in multiple cancers including non-small cell lung cancer (NSCLC). In the search for key genes mediating the aggressive phenotype caused by ARID1A loss, we analyzed 3 Gene Expression Omnibus (GEO) datasets that contain RNA sequencing data from ARID1A-depleted cancer cells. PLAU was identified as a common gene that was induced in different cancer cells upon ARID1A depletion. Overexpression of PLAU positively modulated NSCLC cell growth, colony formation, cisplatin resistance, and survival under serum deprivation. Moreover, enforced expression of PLAU enhanced tumorigenesis of NSCLC cells in nude mice. Mechanistically, PLAU interacted with TM4SF1 to promote the activation of Akt signaling. TM4SF1-overexpressing NSCLC cells resembled those with PLAU overepxression. Knockdown of TM4SF1 inhibited the growth and survival and increased cisplatin sensitivity in NSCLC cells. The interaction between PLAU and TM4SF1 led to the activation of Akt signaling that endowed ARID1A-depleted NSCLC cells with aggressive properties. In addition, treatment with anti-TM4SF1 neutralizing antibody reduced the growth, cisplatin resistance, and tumorigenesis of ARID1A-depleted NSCLC cells. Taken together, PLAU serves as a target gene of ARID1A and promotes NSCLC growth, survival, and cisplatin resistance by stabilizing TM4SF1. Targeting TM4SF1 may be a promising therapeutic strategy for ARID1A-mutated NSCLC. [ABSTRACT FROM AUTHOR]