HHLA2: An Emerging Immune Checkpoint for Cancer Immunotherapy.

HHLA2, a member of the B7 family of co-signaling molecules, is aberrantly expressed in various human cancers and has emerged as a promising target for cancer immunotherapy. It exhibits a unique structure and tissue distribution pattern compared to other B7 family members, where its expression is regulated by the complex physiological and tumor microenvironment. HHLA2 plays a crucial but contradictory role in immune modulation, and is thereby associated with heterogeneous prognostic implications across different cancer types. It interacts with two distinct receptors: TMIGD2, which is predominantly expressed on naïve T and NK cells to deliver co-stimulatory signals to T cells and NK cells; and KIR3DL3, which is prevalent on terminally differentiated T and CD56dim CD16+ NK cells to transmit inhibitory signals. The expression dynamics of these receptors on immune cells contribute to the maintenance of immune response homeostasis. Therapeutic strategies targeting the HHLA2 immune checkpoint aim to selectively inhibit the immunosuppressive HHLA2-KIR3DL3 pathway while preserving the HHLA2-TMIGD2 signaling. Several anti-HHLA2 and anti-KIR3DL3 antibodies are currently under investigation in early clinical trials, building upon encouraging results observed in humanized mouse models. Notably, the non-overlapping expression of HHLA2 and PD-L1 in tumors suggests potential synergistic benefits of combining HHLA2-KIR3DL3 targeted therapies with PD-1/PD-L1 blockade or anti-CTLA-4 to augment antitumor activity.

Natural variation in BnaA07.MKK9 confers resistance to Sclerotinia stem rot in oilseed rape.

Sclerotinia stem rot (SSR), caused by the necrotrophic fungus Sclerotinia sclerotiorum, is one of the most devastating diseases for several major oil-producing crops. Despite its impact, the genetic basis of SSR resistance in plants remains poorly understood. Here, through a genome-wide association study, we identify a key gene, BnaA07. MKK9, that encodes a mitogen-activated protein kinase kinase that confers SSR resistance in oilseed rape. Our functional analyses reveal that BnaA07.MKK9 interacts with BnaC03.MPK3 and BnaC03.MPK6 and phosphorylates them at the TEY activation motif, triggering a signaling cascade that initiates biosynthesis of ethylene, camalexin, and indole glucosinolates, and promotes accumulation of H2O2 and the hypersensitive response, ultimately conferring resistance. Furthermore, variations in the coding sequence of BnaA07.MKK9 alter its kinase activity and improve SSR resistance by ~30% in cultivars carrying the advantageous haplotype. These findings enhance our understanding of SSR resistance and may help engineer novel diversity for future breeding of oilseed rape.

Genome-wide investigation of HD-ZIP gene family and functional characterization of BnaHDZ149 and BnaHDZ22 in salt and drought response in Brassica napus L.

HD-ZIP proteins comprise a plant-specific transcription factor family, which play pivotal roles in plant development and adaptation to ever-changing environment. Although HD-ZIP family members have been identified in some plant species, so far our knowledge about HD-ZIP genes in rapeseed is still limited. In this study, 178 Brassica napus HD-ZIP (BnaHDZ) family members were identified in the rapeseed genome. The phylogenetic relationship, chromosomal locations, intron-exon structures, motif composition, and expression patterns of the BnaHDZ members were analyzed. The BnaHDZ family can be phylogenetically divided into four categories (Ⅰ, Ⅱ, Ⅲ and Ⅳ). Genome-wide transcriptome analysis revealed that most of the HD-ZIP I members respond to at least one abiotic stress. Two closely homologous stress-responsive HD-ZIP Ⅰ genes, BnaHDZ22 and BnaHDZ149, were identified to be involved in drought and salt responses, and selected for further functional characterization. Overexpressing BnaHDZ149 in rapeseed increased salt sensitivity of the transgenic plants, whereas overexpressing BnaHDZ22 increased sensitivity of the transgenic plants to polyethylene glycol (PEG)-simulated drought stress. This research provides not only a comprehensive landscape of BnaHDZ genes, but also a theoretical basis for elucidating the molecular mechanism of the abiotic stress responses of the HD-ZIP family in rapeseed.

Optimizing breast cancer diagnosis with photoacoustic imaging: An analysis of intratumoral and peritumoral radiomics.

Background: The differentiation between benign and malignant breast tumors extends beyond morphological structures to encompass functional alterations within the nodules. The combination of photoacoustic (PA) imaging and radiomics unveils functional insights and intricate details that are imperceptible to the naked eye. Purpose: This study aims to assess the efficacy of PA imaging in breast cancer radiomics, focusing on the impact of peritumoral region size on radiomic model accuracy. Materials and methods: From January 2022 to November 2023, data were collected from 358 patients with breast nodules, diagnosed via PA/US examination and classified as BI-RADS 3-5. The study used the largest lesion dimension in PA images to define the region of interest, expanded by 2 mm, 5 mm, and 8 mm, for extracting radiomic features. Techniques from statistics and machine learning were applied for feature selection, and logistic regression classifiers were used to build radiomic models. These models integrated both intratumoral and peritumoral data, with logistic regressions identifying key predictive features. Results: The developed nomogram, combining 5 mm peritumoral data with intratumoral and clinical features, showed superior diagnostic performance, achieving an AUC of 0.950 in the training cohort and 0.899 in validation. This model outperformed those based solely on clinical features or other radiomic methods, with the 5 mm peritumoral region proving most effective in identifying malignant nodules. Conclusion: This research demonstrates the significant potential of PA imaging in breast cancer radiomics, especially the advantage of integrating 5 mm peritumoral with intratumoral features. This approach not only surpasses models based on clinical data but also underscores the importance of comprehensive radiomic analysis in accurately characterizing breast nodules.

Homoeologous exchanges contribute to branch angle variations in rapeseed: Insights from transcriptome, QTL-seq and gene functional analysis.

Branch angle (BA) is a critical morphological trait that significantly influences planting density, light interception and ultimately yield in plants. Despite its importance, the regulatory mechanism governing BA in rapeseed remains poorly understood. In this study, we generated 109 transcriptome data sets for 37 rapeseed accessions with divergent BA phenotypes. Relative to adaxial branch segments, abaxial segments accumulated higher levels of auxin and exhibited lower expression of six TCP1 homologues and one GA20ox3. A co-expression network analysis identified two modules highly correlated with BA. The modules contained homologues to known BA control genes, such as FUL, YUCCA6, TCP1 and SGR3. Notably, a homoeologous exchange (HE), occurring at the telomeres of A09, was prevalent in large BA accessions, while an A02-C02 HE was common in small BA accessions. In their corresponding regions, these HEs explained the formation of hub gene hotspots in the two modules. QTL-seq analysis confirmed that the presence of a large A07-C06 HE (~8.1 Mb) was also associated with a small BA phenotype, and BnaA07.WRKY40.b within it was predicted as candidate gene. Overexpressing BnaA07.WRKY40.b in rapeseed increased BA by up to 20°, while RNAi- and CRISPR-mediated mutants (BnaA07.WRKY40.b and BnaC06.WRKY40.b) exhibited decreased BA by up to 11.4°. BnaA07.WRKY40.b was exclusively localized to the nucleus and exhibited strong expression correlations with many genes related to gravitropism and plant architecture. Taken together, our study highlights the influence of HEs on rapeseed plant architecture and confirms the role of WRKY40 homologues as novel regulators of BA.

Carnitine metabolites and cognitive improvement in patients with schizophrenia treated with olanzapine: a prospective longitudinal study.

Objective: Cognitive impairment is one of the core symptoms of schizophrenia, which is stable and lifelong. L-carnitine has been shown to improve cognitive function and decrease the rate of cognitive deterioration in patients with Alzheimer's disease. However, it remains unclear regarding the role of L-carnitine and its metabolites in cognitive functions in schizophrenia after treatment with olanzapine. The purpose of this study was to evaluate the relationship between changes in plasma levels of L-carnitine metabolites and cognitive improvement after olanzapine treatment. Methods: This was a prospective longitudinal study. In this study, we recruited 25 female patients with first episode schizophrenia (FES) who were drug naïve at baseline and received 4 weeks of olanzapine monotherapy. Cognitive function was assessed at baseline and 4-week follow-up using the RBANS. Plasma L-carnitine metabolite levels were determined by a metabolomics technology based on untargeted ultra-performance liquid chromatography-mass spectrometry (UPLC-MS). Results: We found that the immediate memory index, delayed memory index and RBANS composite score were significantly increased at the 4-week follow-up after treatment. A total of 7 differential L-carnitine metabolites were identified in FES patients after olanzapine monotherapy. In addition, we found that changes in butyrylcarnitine were positively correlated with improvements in language index and RBANS composite score. Further regression analyses confirmed the association between reduced butyrylcarnitine levels and cognitive improvement after olanzapine monotherapy in FES patients. Conclusion: Our study shows that cognitive improvement after olanzapine treatment was associated with changes in L-carnitine metabolite levels in patients with FES, suggesting a key role of L-carnitine in cognition in schizophrenia.

Concordance of Abundance for Mutational EGFR and Co-Mutational TP53 with Efficacy of EGFR-TKI Treatment in Metastatic Patients with Non-Small-Cell Lung Cancer.

The present study aimed to investigate the influence of the mutation abundance of the epidermal growth factor receptor (EGFR) and its co-mutation with TP53 on the therapeutic efficacy of tyrosine kinase inhibitor (TKI) treatment in patients with metastatic lung adenocarcinoma (LUAD). In total, 130 patients (January 2018-September 2022) with metastatic LUAD from the Second Affiliated Hospital of Zhejiang University were included. Kaplan-Meier analysis was performed to measure the duration of drug application (DDA) and the log-rank test was used to compare differences. Univariate and multivariate analyses of Cox proportional hazard regression models were used to evaluate the association between the relevant clinicopathological factors and DDA. Hazard ratios with 95% confidence intervals were also calculated. Among the 130 patients who were treated with first-generation EGFR-TKIs, 86 showed high-EGFR mutation abundance (>22.0%) and 44 showed low-EGFR mutation abundance (≤22.0%). Patients in the high-EGFR group had a greater DDA than those in the low-EGFR group (p < 0.05). The results of the subgroup analysis were consistent with those of the total mutation population (exon19: >18.5% vs. ≤18.5%, 14 months vs. 10 months, p = 0.049; exon21: >22.0% vs. ≤22.0%, 15 months vs. 9 months, p = 0.005). In addition, the mutation abundance of TP53 was negatively correlated with the DDA (p < 0.05). Patients in the combination group had a better DDA than those in the monotherapy group (p < 0.05). Subgroup analysis showed that, among the low mutation abundance of the EGFR exon 21 or 19 cohort, the combination group had a better DDA than the monotherapy group (p < 0.05). An EGFR mutation abundance greater than 22.0% was a positive predictor of DDA in patients with metastatic LUAD. However, a TP53 mutation abundance higher than 32.5% could reverse this situation. Finally, first-line treatment with EGFR-TKIs plus chemotherapy is a potential treatment strategy for patients with low-abundance EGFR mutations.

Functional Analysis of Bna-miR399c-PHO2 Regulatory Module Involved in Phosphorus Stress in Brassica napus.

Phosphorus stress is one of the important factors restricting plant growth and development, and the microRNA (miRNA) family is involved in the regulation of the response to plant nutrient stress by repressing the expression of target genes at the post-transcriptional or translational level. miR399 is involved in the transportation of phosphate in multiple plants by improving tolerance to low Pi conditions. However, the effect of miR399 on the response of low Pi stress in rapeseed (Brassica napus L.) is unclear. The present study showed a significant increase in taproot length and lateral root number of plants overexpressing Bna-miR399c, while the biomass and Pi accumulation in shoots and roots increased, and the anthocyanin content decreased and chlorophyll content improved under low Pi stress. The results illustrate that Bna-miR399c could enhance the uptake and transportation of Pi in soil, thus making B. napus more tolerant to low Pi stress. Furthermore, we confirmed that BnPHO2 is one of the targets of Bna-miR399c, and the rejection of Pi in rapeseed seedlings increased due to the overexpression of BnPHO2. Hence, we suggest that miR399c-PHO2 module can effectively regulate the homeostasis of Pi in B. napus. Our study can also provide the theoretical basis for germplasm innovation and the design of intelligent crops with low nutrient input and high yield to achieve the dual objectives of income and yield increase and environmental protection in B. napus.

Mutant NPM1 maintains RASGRP3 protein stability via interaction with MID1 to promote acute myeloid leukemia cell proliferation and autophagy.

Acute myeloid leukemia is a heterogeneous hematologic malignancy with high mortality in the world. NPM1 gene mutations are a frequent occurrence in acute myeloid leukemia, leading to abnormal autophagy, while the mechanism of NPM1 mutation-driven acute myeloid leukemia pathogenesis remains to be fully elucidated. GEO microarrays were used to screen for dysregulated autophagy-related genes in NPM1-mutant acute myeloid leukemia and analysis of RASGRP3 expression and prognosis. Next, we explored the potential molecular mechanisms relationship between RASGRP3 and NPM1 through utilizing immunoprecipitation, Western blot, and cycloheximide assay. Further, CCK8, EdU staining, immunofluorescence, and Western blot were performed to explore the effect of RASGRP3 on cell proliferation and apoptosis in NPM1-mutated acute myeloid leukemia. Finally, Western blot was used to study the mechanism of action of RASGRP3. RASGRP3 expression was upregulated in NPM1-mutated acute myeloid leukemia. Mislocalized NPM1-mA in the cytoplasm could bind to E3 ubiquitin-protein ligase MID1 to block degradation of the RASGRP3 protein. RASGRP3 could also activate the EGFR-STAT3 axis to promote proliferation and autophagy in acute myeloid leukemia. In conclusion, our results identified RASGRP3 as a proto-oncogene in NPM1-mutated acute myeloid leukemia. The RASGRP3-EGFR/STAT3 axis may be a promising therapeutic target for this unique leukemic subtype.

[Effect of astragaloside â £ on angiotensin â ¡-induced inflammatory response of vascular endothelial cells and mechanism].

This study was designed to determine the inhibitory effect of astragaloside Ⅳ(AS-Ⅳ), a principal bioactive component extracted from the Chinese medicinal Astragali Radix, on the inflammatory response of vascular endothelial cells induced by angiotensin Ⅱ(Ang Ⅱ), the most major pathogenic factor for cardiovascular diseases, and to clarify the role of calcium(Ca~(2+))/phosphatidylinosi-tol-3-kinase(PI3K)/protein kinase B(Akt)/endothelial nitric oxide synthase(eNOS)/nitric oxide(NO) pathway in the process. To be specific, human umbilical vein endothelial cells(HUVECs) were cultured in the presence of AS-Ⅳ with or without the specific inhibitor of NO synthase(NG-monomethyl-L-arginine, L-NMMA), inhibitor of PI3K/Akt signaling pathway(LY294002), or Ca~(2+)-chelating agent(ethylene glycol tetraacetic acid, EGTA) prior to Ang Ⅱ stimulation. The inhibitory effect of AS-Ⅳ on Ang Ⅱ-induced inflammatory response and the involved mechanism was determined with enzyme-linked immunosorbent assay(ELISA), cell-based ELISA assay, Western blot, and monocyte adhesion assay which determined the fluorescently labeled human monocytic cell line(THP-1) adhered to Ang Ⅱ-stimulated endothelial cells. AS-Ⅳ increased the production of NO by HUVECs in a dose-and time-dependent manner(P<0.05) and raised the level of phosphorylated eNOS(P<0.05). The above AS-Ⅳ-induced changes were abolished by pretreatment with L-NMMA, LY294002, or EGTA. Compared with the control group, Ang Ⅱ obviously enhanced the production and release of cytokines(tumor necrosis factor-α, interleukin-6), chemokines(monocyte chemoattractant protein-1) and adhesion molecules(intercellular adhesion molecule-1, vascular cellular adhesion molecule-1), and the number of monocytes adhered to HUVECs(P<0.05), which were accompanied by the enhanced levels of phosphorylated inhibitor of nuclear factor-κBα protein and activities of nuclear factor-κB(NF-κB)(P<0.05). This study also demonstrated that Ang Ⅱ-induced inflammatory response was inhibited by pretreatment with AS-Ⅳ(P<0.05). In addition, the inhibitory effect of AS-Ⅳ was abrogated by pretreatment with L-NMMA, LY294002, or EGTA(P<0.05). This study provides a direct link between AS-Ⅳ and Ca~(2+)/PI3K/Akt/eNOS/NO pathway in AS-Ⅳ-mediated anti-inflammatory actions in endothelial cells exposed to Ang Ⅱ. The results indicate that AS-Ⅳ attenuates endothelial cell-mediated inflammatory response induced by Ang Ⅱ via the activation of Ca~(2+)/PI3K/Akt/eNOS/NO signaling pathway.

Diachronic shifts in lithic technological transmission between the eastern Eurasian Steppe and northern China in the Late Pleistocene.

The successful occupation of the eastern Eurasian Steppe in the Late Pleistocene improved cultural connections between western Eurasia and East Asia. We document multiple waves of lithic technological transmission between the eastern Eurasian Steppe and northern China during 50-11 cal. ka BP. These waves are apparent in the sequential appearance of three techno-complexes in northern China: (1) the Mousterian techno-complex, (2) the blade techno-complex mixed with Mousterian elements, (3) and the microlithized blade techno-complex. These lithic techno-complexes were transmitted under different paleoenvironmental conditions along different pathways through the eastern Eurasian Steppe. The Mousterian techno-complex and the blade techno-complex mixed with Mousterian elements were only dispersed in the north and west peripheries of northern China (50-33 cal. ka BP). We argue that these techno-complexes failed to penetrate into the hinterland of northern China because they were not well suited to local geographical conditions. In contrast, the microlithized blade technology which diffused from the eastern Eurasian Steppe was locally modified into a Microblade techno-complex which was highly suited to local environmental conditions, and proliferated across the hinterland of northern China (28/27-11 cal. ka BP). The subsequent spread of microblade technology over vast regions of Mongolia and Siberia indicates that the Pleistocene inhabitants of northern China not only adopted and modified technologies from their neighbors in the Eurasian Steppe, but these modified variants were subsequently transmitted back into the Eurasian Steppe. These episodes of technological transmission indicate complicated patterns of population dispersal and technological interaction across northern China and the eastern Eurasian Steppe.

Multiple Functions of MiRNAs in Brassica napus L.

The worldwide climate changes every year due to global warming, waterlogging, drought, salinity, pests, and pathogens, impeding crop productivity. Brassica napus is one of the most important oil crops in the world, and rapeseed oil is considered one of the most health-beneficial edible vegetable oils. Recently, miRNAs have been found and confirmed to control the expression of targets under disruptive environmental conditions. The mechanism is through the formation of the silencing complex that mediates post-transcriptional gene silencing, which pairs the target mRNA and target cleavage and/or translation inhibition. However, the functional role of miRNAs and targets in B. napus is still not clarified. This review focuses on the current knowledge of miRNAs concerning development regulation and biotic and abiotic stress responses in B. napus. Moreover, more strategies for miRNA manipulation in plants are discussed, along with future perspectives, and the enormous amount of transcriptome data available provides cues for miRNA functions in B. napus. Finally, the construction of the miRNA regulatory network can lead to the significant development of climate change-tolerant B. napus through miRNA manipulation.

An R3-MYB repressor, BnCPC forms a feedback regulation with MBW complex to modulate anthocyanin biosynthesis in Brassica napus.

BACKGROUND: Anthocyanins are metabolites of phenylpropanoid pathway, and involves in diverse processes of plant development and adaptation, which are regulated by the MYB-bHLH-WD40 (MBW) protein complexes. Many R2R3-MYB activators have been well characterized, but the MYB repressors in anthocyanin biosynthesis were recognized recently, which are also important in modulating phenylpropanoid metabolism in plants. The regulatory mechanism of anthocyanin biosynthesis in oil crop Brassica napus remains to be revealed. RESULTS: In this study, we identified an anthocyanin repressor BnCPC in B. napus. BnCPC encoded a typical R3-MYB protein containing a conserved [D/E]Lx2[R/K]x3Lx6Lx3R motif for interaction with bHLH proteins. Overexpression of BnCPC in B. napus inhibited anthocyanin accumulation, especially under anthocyanin inducible conditions. Protein-protein interaction and dual-luciferase assays confirmed that BnCPC could compete with BnPAP1 to interact with bHLHs (BnTT8 and BnEGL3), and repress the expression of anthocyanin biosynthetic genes (e.g., BnDFR) that activated by MBW complexes. Moreover, we found BnCPC inhibited the MBW complex-induced BnCPC activity. CONCLUSIONS: Overall, this research demonstrated that BnCPC repressed anthocyanin biosynthesis by affecting the formation of MBW complex, and formed a feedback loop to regulate anthocyanin accumulation in B. napus.

Triptolide Alleviates Oxidized LDL-Induced Endothelial Inflammation by Attenuating the Oxidative Stress-Mediated Nuclear Factor-Kappa B Pathway.

Background: Endothelial inflammation triggered by oxidized LDL (ox-LDL) is a crucial mechanism involved in atherosclerosis. Triptolide (TP), a primary active ingredient of the traditional Chinese medicine Tripterygium wilfordii Hook F, possesses antioxidant and anti-inflammatory properties in vivo. However, limited information is available regarding these effects on endothelial inflammation occurring in atherosclerosis. Objectives: This study investigated the effects and possible mechanisms of action of TP on ox-LDL-induced inflammatory responses in human umbilical vein endothelial cells. Methods: Human umbilical vein endothelial cells were preincubated with TP at the indicated concentrations for 1 hour and then incubated with ox-LDL (50 µg/mL) for the indicated times. Results: Preincubation of cultured human umbilical vein endothelial cells with TP inhibited ox-LDL-induced cytokine and chemokine production, adhesion molecule expression, and monocyte adhesion in a concentration-dependent manner. The concentrations of 8-isoprostane, malondialdehyde, and superoxide increased after human umbilical vein endothelial cells were exposed to ox-LDL, which were associated with decreased activities of total superoxide dismutase and its isoenzyme (ie, CuZn- superoxide dismutase). Preincubation with TP reversed ox-LDL-induced effects in all events. Moreover, preincubation with TP also attenuated ox-LDL-induced nuclear factor-kappa B transcriptional activation in a concentration-dependent manner, via the suppression of inhibitor of kappa Balpha (IκBα) phosphorylation and subsequent nuclear factor-kappa B DNA binding. Conclusions: These data indicate that TP inhibits ox-LDL-induced endothelial inflammation, possibly via suppression of the oxidative stress-dependent activation of the nuclear factor-kappa B signaling pathway.

Genome-wide analysis of the G-box regulating factors protein family reveals its roles in response to Sclerotinia sclerotiorum infection in rapeseed (Brassica napus L.).

The G-box regulating factors (GRFs) are involved in a wide array of signal transduction pathway and play important roles in plant physiological and developmental processes and stress responses. The GRF proteins have previously been described in several plant species, but not in rapeseed (Brassica napus L.). In this study, we carried out genome-wide analysis of GRFs in B. napus based on the available genome sequence information, and analyzed their expression in different tissues under different hormone treatments and after inoculation with Sclerotinia sclerotiorum. We identified 46 putative BnaGRF genes in rapeseed, unevenly distributed on 18 chromosomes. Like the 14-3-3 proteins in other plant species, the 46 putative BnaGRFs could be classified into two major evolutionary branches: epsilon (ε) group and non-epsilon (non-ε) group. Evolutionary analysis indicated that the BnaGRF gene family expanded in both groups much before speciation. We discovered an expansion of the 14-3-3 gene family that likely occurred during a recent gene duplication event. Collinearity analysis revealed that most of the BnaGRF genes shared syntenic relationships. Global gene expression profiling of BnaGRFs by RNA-seq analysis showed 41.3% (19/46) response to S. sclerotiorum infection, and this response was probably mediated through jasmonic acid (JA) and salicylic acid (SA) signaling pathways. These results provide key insights into the role of 14-3-3s in the biotic stress response and enhance our understanding of their multiple functions in B. napus.

The Sclerotinia sclerotiorum-inducible promoter pBnGH17D7 in Brassica napus: isolation, characterization, and application in host-induced gene silencing.

Sclerotinia stem rot (SSR), caused by Sclerotinia sclerotiorum, is among the most devastating diseases in Brassica napus worldwide. Conventional breeding for SSR resistance in Brassica species is challenging due to the limited availability of resistant germplasm. Therefore, genetic engineering is an attractive approach for developing SSR-resistant Brassica crops. Compared with the constitutive promoter, an S. sclerotiorum-inducible promoter would avoid ectopic expression of defense genes that may cause plant growth deficits. In this study, we generated a S. sclerotiorum-inducible promoter. pBnGH17D7, from the promoter of B. napus glycosyl hydrolase 17 gene (pBnGH17). Specifically, 5'-deletion and promoter activity analyses in transgenic Arabidopsis thaliana plants defined a 189 bp region of pBnGH17 which was indispensable for S. sclerotiorum-induced response. Compared with pBnGH17, pBnGH17D7 showed a similar response upon S. sclerotiorum infection, but lower activity in plant tissues in the absence of S. sclerotiorum infection. Moreover, we revealed that the transcription factor BnTGA7 directly binds to the TGACG motif in pBnGH17D7 to activate BnGH17. Ultimately, pBnGH17D7 was exploited for engineering Sclerotinia-resistant B. napus via host-induced gene silencing. It induces high expression of siRNAs against the S. sclerotiorum pathogenic factor gene specifically during infection, leading to increased resistance.

Genome-Wide Analysis of the Type-B Authentic Response Regulator Gene Family in Brassica napus.

The type-B authentic response regulators (type-B ARRs) are positive regulators of cytokinin signaling and involved in plant growth and stress responses. In this study, we used bioinformatics, RNA-seq, and qPCR to study the phylogenetic and expression pattern of 35 type-B ARRs in Brassica napus. The BnARRs experienced gene expansion and loss during genome polyploidization and were classified into seven groups. Whole-genome duplication (WGD) and segmental duplication were the main forces driving type-B ARR expansion in B. napus. Several BnARRs with specific expression patterns during rapeseed development were identified, including BnARR12/14/18/23/33. Moreover, we found the type-B BnARRs were involved in rapeseed development and stress responses, through participating in cytokinin and ABA signaling pathways. This study revealed the origin, evolutionary history, and expression pattern of type-B ARRs in B. napus and will be helpful to the functional characterization of BnARRs.

The miR393-Target Module Regulates Plant Development and Responses to Biotic and Abiotic Stresses.

MicroRNAs (miRNAs), a class of endogenous small RNAs, are broadly involved in plant development, morphogenesis and responses to various environmental stresses, through manipulating the cleavage, translational expression, or DNA methylation of target mRNAs. miR393 is a conserved miRNA family present in many plants, which mainly targets genes encoding the transport inhibitor response1 (TIR1)/auxin signaling F-box (AFB) auxin receptors, and thus greatly affects the auxin signal perception, Aux/IAA degradation, and related gene expression. This review introduces the advances made on the miR393/target module regulating plant development and the plant's responses to biotic and abiotic stresses. This module is valuable for genetic manipulation of optimized conditions for crop growth and development and would also be helpful in improving crop yield through molecular breeding.

The Pyramiding of Three Key Root Traits Aid Breeding of Flood-Tolerant Rice.

Flooding is constantly threatening the growth and yield of crops worldwide. When flooding kicks in, the soil becomes water-saturated and, therefore, the roots are the first organs to be exposed to excess water. Soon after flooding, the soil turns anoxic and the roots can no longer obtain molecular oxygen for respiration from the rhizosphere, rendering the roots dysfunctional. Rice, however, is a semi-aquatic plant and therefore relatively tolerant to flooding due to adaptive traits developed during evolution. In the present review, we have identified three key root traits, viz. cortical aerenchyma formation, a barrier to radial oxygen loss and adventitious root growth. The understanding of the physiological function, the molecular mechanisms, and the genetic regulation of these three traits has grown substantially and therefore forms the backbone of this review. Our synthesis of the recent literature shows each of the three key root traits contributes to flood tolerance in rice. One trait, however, is generally insufficient to enhance plant tolerance to flooding. Consequently, we suggest comprehensive use of all three adaptive traits in a pyramiding approach in order to improve tolerance to flooding in our major crops, in general, and in rice, in particular.