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Due to the COVID-19 pandemic, the presentation of public health data to lay audiences has increased without most people having the knowledge to understand what these statistics mean. Recognizing that minoritized populations are deeply impacted by the pandemic and wanting to improve the racial representation in biostatistics we developed a training program aimed at increasing the data literacy of high school and college students from minoritized groups. The program introduced the basics of public health, data literacy, statistical software, descriptive statistics, and data ethics. The instructors taught eight synchronous sessions consisting of lectures and experiential group exercises. Five of the sessions were also offered asynchronously. Of the 209 students, 76% were college students; 90% identified as Black, Asian, or Latino/a/x; and the average age was 21 years. In synchronous sessions, 56% of students attended all sessions. All course sessions were rated as good/excellent by most ([Formula: see text]) students. The program recruited, engaged, and retained a large cohort ([Formula: see text]) of underrepresented students in biostatistics/data science for a virtual data literacy training. The program demonstrates the feasibility of developing and implementing public health training programs designed to increase racial and gender diversity in the field.

Mutation of the MAPK7 gene was related to human scoliosis. Mapk7 regulated the development of limb bones and skulls in mice. However, the role of MAPK7 in vertebral development is still unclear. In this study, we constructed Col2a1-cre; Mapk7f/f transgenic mouse model to delete Mapk7 in cartilage, which displayed kyphosis and osteopenia. Mechanistically, Mapk7 loss decreased MEF2C expression and thus activated PTEN to oppose PI3K/AKT signaling in vertebral growth plate chondrocytes, which impaired chondrocyte hypertrophy and attenuated vertebral ossification. In vivo, systemic pharmacological activation of AKT rescued impaired chondrocyte hypertrophy and alleviated mouse vertebral defects caused by Mapk7 deficiency. Our study firstly clarified the mechanism by which MAPK7 was involved in vertebral development, which might contribute to understanding the pathology of spinal deformity and provide a basis for the treatment of developmental disorders of the spine.

The heading date, a critical trait influencing the rice yield and quality, has always been a hot topic in breeding research. Appropriately delaying the flowering time of excellent northern rice varieties is of great significance for improving yields and enhancing regional adaptability during the process for introducing varieties from north to south. In this study, genes influencing the heading date were identified through genome-wide association studies (GWAS). Using KenDao 12 (K12), an excellent cultivar from northern China, as the material, the specific flowering activator, OsMADS50, was edited using the genome-editing method to regulate the heading date to adapt to the southern planting environment. The results indicated that the osmads50 mutant line of K12 flowered about a week later, with a slight increase in the yield and good adaptability in the southern region in China. Additionally, the expressions of key flowering regulatory genes, such as Hd1, Ghd7, Ehd1, Hd3a, and RFT1, were reduced in the mutant plants, corroborating the delayed flowering phenotype. Yield trait analysis revealed that the primary factor for improved yield was an increase in the number of effective tillers, although there is potential for further enhancements in the seed-setting rate and grain plumpness. Furthermore, there were significant increases in the length-to-width ratio of the rice grains, fat content, and seed transparency, all contributing to an overall improvement in the rice quality. In summary, this study successfully obtained a rice variety with a delayed growth period through OsMADS50 gene editing, effectively implementing the strategy for adapting northern rice varieties to southern climates. This achievement significantly supports efforts to enhance the rice yield and quality as well as to optimize production management practices.

Abstract Metabolic reprogramming and epigenetic modifications are hallmarks of cancer cells. In cancer cells, metabolic pathway activity varies during tumorigenesis and cancer progression, indicating regulated metabolic plasticity. Metabolic changes are often closely related to epigenetic changes, such as alterations in the expression or activity of epigenetically modified enzymes, which may exert a direct or an indirect influence on cellular metabolism. Therefore, exploring the mechanisms underlying epigenetic modifications regulating the reprogramming of tumor cell metabolism is important for further understanding tumor pathogenesis. Here, we mainly focus on the latest studies on epigenetic modifications related to cancer cell metabolism regulations, including changes in glucose, lipid and amino acid metabolism in the cancer context, and then emphasize the mechanisms related to tumor cell epigenetic modifications. Specifically, we discuss the role played by DNA methylation, chromatin remodeling, noncoding RNAs and histone lactylation in tumor growth and progression. Finally, we summarize the prospects of potential cancer therapeutic strategies based on metabolic reprogramming and epigenetic changes in tumor cells.

Background: In recent years, fracture liaison services (FLS) have been applied for hip fractures; however, their effectiveness remains uncertain. Objective: To evaluate the effectiveness of FLS in patients with hip fractures. Design: A systematic review and meta-analysis of randomized controlled trials. Data sources: Embase, PubMed, Cochrane Library, Ebsco, Ovid, Web of Science, Medline, CNKI, Wangfang, and Vip were searched from their date of inception to March 2023. Two researchers screened the literature based on the inclusion and exclusion criteria, evaluated the quality, extracted data, and conducted a meta-analysis using ReviewManager 5.4. Results: After screening, 12 randomised controlled trials (RCT) including 2136 patients were used in the meta-analysis. The primary outcomes were hip function rate of recurrent fracture, medication adherence, and degree of weakness. FLS improved hip function in patients with hip fractures [MD = 9.37, 95 % CI (7.69, 11.06), P

Epithelioid inflammatory myofibroblastic sarcoma (EIMS) is a highly aggressive malignant subtype of inflammatory myofibroblastoma (IMT) associated with poor prognosis. IMT can occur in various parts of the body, most frequently in the lungs, followed by the mesentery, omentum, retroperitoneum, and pelvis, among other areas; however, it is exceptionally rare in the stomach. Anaplastic lymphoma kinase (ALK) is a critical driver of lung cancer development and is currently the “gold standard” target for non-small cell lung cancer treatment. However, there are few reports on the use of ALK inhibitors for EIMS, necessitating further investigation. A male patient with postoperative inflammatory myofibroblastic sarcoma of the stomach received postoperative chemotherapy and had a stable outcome. However, a repeat CT scan performed 11 months later revealed disease progression. The patient later underwent immunohistochemistry testing that indicated ALK positivity, and next-generation sequencing revealed STRN-ALK fusion. Ensartinib 225 mg qd was administered as recommended, and the patient experienced only mild pruritus and no adverse effects such as rash. Eight months after CT follow-up, the patient’s subseptal soft tissue nodules had decreased, and the outcome was assessed as a partial response. The findings of this case report introduce a novel strategy for treating ALK-positive EIMS that utilizes ensartinib, a drug with previously demonstrated success in the treatment of ALK-positive cancer.

Purpose – This paper theoretically and empirically analyzes the effects of the elderly’s physical health status on their need for care and the choice of care models in China. Design/methodology/approach – Empirically, the estimation results of a large-sample randomized intervention trial with chronic obstructive pulmonary disease (COPD) patients through the difference-in-difference method indicated the following: (1) After the COPD intervention trial, the physical health status of the elderly in the treatment group improved significantly, the need for care was substantially reduced and the health improvement led to a 35.5% reduction in the probability of using elderly care. (2) The reduction in the need for care regarding the treatment group occurred mainly in social care. The probability of using social care decreased by 67.8% due to the elderly’s health improvement, while that of home care remained unchanged generally. (3) Further heterogeneity tests suggested that families with fewer potential internal resources for caregiving had a more pronounced decline in the need for social care. Findings – Theoretically, these empirical results support the existence of the “pecking order” theory in the family’s choice of elderly care model, that is, families tend to employ all internal resources for caregiving before resorting to social care, resulting in a higher sensitivity of social care to health. Originality/value – The main policy implication of this paper is that ex ante preventive health intervention policies can significantly alleviate the burden of care, especially social care, on families. And preventive health intervention policies are particularly effective in reducing the burden of the families with relatively few resources for informal internal care.

Abstract The harmonious functioning of growth plate chondrocytes is crucial for skeletogenesis. These cells rely on an appropriate intensity of glycolysis to maintain survival and function in an avascular environment, but the underlying mechanism is poorly understood. Here we show that Hnrnpk orchestrates growth plate development by maintaining the appropriate intensity of glycolysis in chondrocytes. Ablating Hnrnpk causes the occurrence of dwarfism, exhibiting damaged survival and premature differentiation of growth plate chondrocytes. Furthermore, Hnrnpk deficiency results in enhanced transdifferentiation of hypertrophic chondrocytes and increased bone mass. In terms of mechanism, Hnrnpk binds to Hif1a mRNA and promotes its degradation. Deleting Hnrnpk upregulates the expression of Hif1α, leading to the increased expression of downstream glycolytic enzymes and then exorbitant glycolysis. Our study establishes an essential role of Hnrnpk in orchestrating the survival and differentiation of chondrocytes, regulating the Hif1α-glycolysis axis through a post-transcriptional mechanism during growth plate development.

Abstract The intervertebral disc (IVD) acts as a fibrocartilaginous joint to anchor adjacent vertebrae. Although several studies have demonstrated the cellular heterogeneity of adult mature IVDs, a single‐cell transcriptomic atlas mapping early IVD formation is still lacking. Here, the authors generate a spatiotemporal and single cell‐based transcriptomic atlas of human IVD formation at the embryonic stage and a comparative mouse transcript landscape. They identify two novel human notochord (NC)/nucleus pulposus (NP) clusters, SRY‐box transcription factor 10 (SOX10)+ and cathepsin K (CTSK)+, that are distributed in the early and late stages of IVD formation and they are validated by lineage tracing experiments in mice. Matrisome NC/NP clusters, T‐box transcription factor T (TBXT)+ and CTSK+, are responsible for the extracellular matrix homeostasis. The IVD atlas suggests that a subcluster of the vertebral chondrocyte subcluster might give rise to an inner annulus fibrosus of chondrogenic origin, while the fibroblastic outer annulus fibrosus preferentially expresseds transgelin and fibromodulin . Through analyzing intercellular crosstalk, the authors further find that notochordal secreted phosphoprotein 1 (SPP1) is a novel cue in the IVD microenvironment, and it is associated with IVD development and degeneration. In conclusion, the single‐cell transcriptomic atlas will be leveraged to develop preventative and regenerative strategies for IVD degeneration.

Abstract Ghrelin is the only known orexigenic gut hormone, and its synthesis, secretion and degradation are affected by different metabolic statuses. This meta-analysis aimed to investigate the potential differences in plasma acyl ghrelin (AG) and des-acyl ghrelin (DAG) concentrations between normal weight and obese adults. Systematic literature searches of PubMed, Embase and Web of Science through October 2021 were conducted for articles reporting AG or DAG levels in obesity and normal weight, and 34 studies with 1863 participants who met the eligibility criteria were identified. Standardized mean differences (SMDs) with 95% confidence intervals (CIs) were calculated to evaluate group differences in circulating AG and DAG levels. Pooled effect size showed significantly lower levels of baseline AG (SMD: − 0.85; 95% CI: − 1.13 to − 0.57; P SMD

BackgroundAcute promyelocytic leukemia (APL) is typically characterized by the presence of coagulopathy and the PML::RARA fusion gene. The FIP1L1::RARA has been reported as a novel fusion gene, but studies on its pathogenesis are limited.ObjectivesA FIP1L1::RARA fusion in a child finally diagnosed as APL was reported. RNA sequencing (RNA-seq) of six patients (three cases of acute lymphoblastic leukemia (ALL), one case of myelodysplastic syndrome (MDS), one case of acute megakaryoblastic leukemia (M7), and one case of APL with FIP1L1::RARA) were performed.MethodsTranscriptome analysis of six patients was performed by RNA-seq. The heat map was used for showing the RNA expression profile, the volcano plot for identifying differential expression genes (DEGs), and the KEGG Orthology-Based Annotation System (KOBAS) online biological information database for KEGG pathway enrichment analysis.ResultsObvious differences between APL with FIP1L1::RARA and hematologic malignancies were identified. 1060 common differentially expressed genes (co-DEGs) were detected between APL with FIP1L1::RARA vs ALL and APL with FIP1L1::RARA vs myeloid neoplasms (MDS, M7), the up-regulated genes were mainly mapped into platelet activation, cancer, AMPK signaling pathway, PI3K-Akt signaling pathway, and MAPK signaling pathway. The down-regulated genes were significantly associated with TNF signaling pathway, Rap1 signaling pathway, Age-RAGE signaling pathway, and apoptosis.ConclusionA FIP1L1::RARA fusion in a child finally diagnosed as APL was reported. RNA-seq may provide a new diagnostic method when RARA rearrangements fail to be identified by conventional methods. In the analysis of co-DEGs between case vs ALL and case vs myeloid neoplasms, the up-regulated and down-regulated genes were enriched in different signaling pathways. Further experimental studies are needed to identify pathogenesis and treatment for APL with FIP1L1::RARA.

Abstract Background Plant cell walls are the main physical barrier encountered by pathogens colonizing plant tissues. Alteration of cell wall integrity (CWI) can activate specific defenses by impairing proteins involved in cell wall biosynthesis, degradation and remodeling, or cell wall damage due to biotic or abiotic stress. Polygalacturonase (PG) depolymerize pectin by hydrolysis, thereby altering pectin composition and structures and activating cell wall defense. Although many studies of CWI have been reported, the mechanism of how PGs regulate cell wall immune response is not well understood. Results Necrosis appeared in leaf tips at the tillering stage, finally resulting in 3–5 cm of dark brown necrotic tissue. ltn-212 showed obvious cell death and accumulation of H2O2 in leaf tips. The defense responses were activated in ltn-212 to resist bacterial blight pathogen of rice. Map based cloning revealed that a single base substitution (G-A) in the first intron caused incorrect splicing of OsPG1, resulting in a necrotic phenotype. OsPG1 is constitutively expressed in all organs, and the wild-type phenotype was restored in complementation individuals and knockout of wild-type lines resulted in necrosis as in ltn-212. Transmission electron microscopy showed that thicknesses of cell walls were significantly reduced and cell size and shape were significantly diminished in ltn-212. Conclusion These results demonstrate that OsPG1 encodes a PG in response to the leaf tip necrosis phenotype of ltn-212. Loss-of-function mutation of ltn-212 destroyed CWI, resulting in spontaneous cell death and an auto-activated defense response including reactive oxygen species (ROS) burst and pathogenesis-related (PR) gene expression, as well as enhanced resistance to Xanthomonas oryzae pv. oryzae (Xoo). These findings promote our understanding of the CWI mediated defense response.

Abstract Background Long bones of limbs are formed through endochondral bone formation, which depends on the coordinated development of growth plates. Our previous studies have demonstrated that dysfunction of mitogen-activated protein kinase 7 (MAPK7) can cause skeletal dysplasia. However, little is known about the role of MAPK7 in the regulation of proliferation and differentiation of chondrocytes during growth plate development. Results Ablation of MAPK7 expression in chondrocytes led to growth restriction, short limbs and bone mass loss in postnatal mice. Histological studies revealed that MAPK7 deficiency increased the apoptosis and decreased the proliferation of chondrocytes in the center of the proliferative layer, where the most highly hypoxic chondrocytes are located. Accordingly, hypertrophic differentiation markers were downregulated in the central hypertrophic layer, beneath the site where abnormal apoptosis was observed. Simultaneously, we demonstrated that hypoxic adaptation and hypoxia-induced activation of hypoxia-inducible factor 1 subunit α (HIF1α) were impaired when MAPK7 could not be activated normally in primary chondrocytes. Concomitantly, vascular invasion into epiphyseal cartilage was inhibited when Mapk7 was deleted. Conclusions We demonstrated that MAPK7 is necessary for maintaining proliferation, survival, and differentiation of chondrocytes during postnatal growth plate development, possibly through modulating HIF1α signaling for adaptation to hypoxia. These results indicate that MAPK7 signaling might be a target for treatment of chondrodysplasia.

Abstract Changes in volatile compounds of fermented minced pepper (FMP) during natural fermentation (NF) and inoculated fermentation (IF) process were analyzed by the headspace–gas chromatography–ion mobility spectrometry (HS‐GC‐IMS). A total of 53 volatile compounds were identified, including 12 esters, 17 aldehydes, 13 alcohols, four ketones, three furans, two acids, one pyrazine, and one ether. Generally, fermentation time played an important role in volatile compounds of FMP. It was found that most esters, aldehydes, and alcohols obviously decreased with the increase in fermentation time, including isoamyl hexanoate, methyl octanoate, gamma‐butyrolactone, phenylacetaldehyde, methional, and E‐2‐hexenol. Only a few volatile compounds increased, especially for 2‐methylbutanoic acid, 2‐methylpropionic acid, linalool, ethanol, and ethyl acetate. However, no significant difference in volatile compounds was found between NF and IF samples at the same fermentation time. In addition, the fermentation process in all samples was well discriminated as three stages (0 days; 6 day; and 12, 18, and 24 days), and all volatile compounds were divided into two categories (increase and decrease) based on principal component analysis and heat map.

A variety of genetic techniques have been devised to determine cell lineage relationships during tissue development. Some of these systems monitor cell lineages spatially and/or temporally without regard to gene expression by the cells, whereas others correlate gene expression with the lineage under study. The GAL4 Technique for Real-time and Clonal Expression (G-TRACE) system allows for rapid, fluorescent protein-based visualization of both current and past GAL4 expression patterns and is therefore amenable to genome-wide expression-based lineage screens. Here we describe the results from such a screen, performed by undergraduate students of the University of California, Los Angeles (UCLA) Undergraduate Research Consortium for Functional Genomics (URCFG) and high school summer scholars as part of a discovery-based education program. The results of the screen, which reveal novel expression-based lineage patterns within the brain, the imaginal disc epithelia, and the hematopoietic lymph gland, have been compiled into the G-TRACE Expression Database (GED), an online resource for use by the Drosophila research community. The impact of this discovery-based research experience on student learning gains was assessed independently and shown to be greater than that of similar programs conducted elsewhere. Furthermore, students participating in the URCFG showed considerably higher STEM retention rates than UCLA STEM students that did not participate in the URCFG, as well as STEM students nationwide.

Automatically and accurately reconstructing the overhead wires of railway from airborne laser scanning (ALS) data are an efficient way of railway monitoring to ensure stable and safety transportation services. However, due to the complex structure of the overhead wires, it is challenging to extract these wires using the existing methods. This work proposes a workflow for railway overhead wire reconstruction using deep learning for wire identification collaborating with the RANdom SAmple Consensus (RANSAC) algorithm for wire reconstruction. First, data augmentation and ground points down-sampling are performed to facilitate the issues caused by insufficient and non-uniformity of LiDAR points. Then, a network incorporating with PointNet model is proposed to segment wires, pylons and ground points. The proposed network is composed of a Geometry Feature Extraction (GFE) module and a Neighborhood Information Aggregation (NIA) module. These two modules are introduced to encode and describe the local geometric features. Therefore, the capability of the model to discriminate geometric details is enhanced. Finally, a wire individualization and multi-wire fitting algorithm is proposed to reconstruct the overhead wires. A number of experiments are conducted using ALS point cloud data of railway scenarios. The results show that the accuracy and MIoU for wire identification are 96.89% and 82.56%, respectively, which demonstrates a better performance compared to the existing methods. The overall reconstruction accuracy is 96% over the study area. Furthermore, the presented strategy also demonstrated its applicability to high-voltage powerline scenarios.

White tea (WT) is a slightly fermented tea, and withering is a critical step in its processing. The withering treatment can affect white tea’s aroma; different treatments’ effects were investigated in this study. White tea was withered indoors (IWT), in a withering-tank (WWT), or under sunlight (SWT). Quantitative descriptive analysis (QDA) results showed that SWT had a more obvious flower aroma, and WWT had a more pronounced grassy aroma. Volatile compounds were extracted and subsequently detected with solvent-assisted flavor evaporation (SAFE) and headspace solid-phase microextraction (HS-SPME) combined in addition to gas chromatography–mass spectrometry (GC-MS). A total of 202 volatile compounds were detected; 35 of these aroma-active compounds met flavor dilution (FD) factor ≥ 4 or odor activity value (OAV) ≥ 1. The nine key potent odorants for which both conditions were met were dimethyl sulfide, 2-methyl-butanal, 1-penten-3-one, hexanal, (Z)-4-heptenal, β-Myrcene, linalool, geraniol, and trans-β-ionone. These results were used with QDA to reveal that SWT had a stronger floral aroma mainly due to an increase of geraniol and linalool. Moreover, WWT had a stronger grassy aroma mainly due to increased hexanal. The results could be used to select processing methods for producing white tea with a superior aroma.

Chlamydia psittaci is an important zoonotic factor associated with human and animal atypical pneumonia. Resisting host cell apoptosis is central to sustaining Chlamydia infection in vivo. Chlamydia can secrete inclusion membrane proteins (Incs) that play important roles in their development cycle and pathogenesis. CPSIT_0846 is an Inc protein in C. psittaci identified by our team in previous work. In the current study, we investigated the regulatory role of CPSIT_0846 in HeLa cell apoptosis, and explored potential mechanisms. The results showed that HeLa cells treated with CPSIT_0846 contained fewer apoptotic bodies and exhibited a lower apoptotic rate than untreated cells either with Hoechst 33258 fluorescence staining or flow cytometry with or without induction by staurosporine (STS). CPSIT_0846 could increase the phosphorylation of the extracellular signal-regulated kinases 1/2 (ERK1/2) or stress-activated protein kinases/c-Jun amino-terminal kinases (SAPK/JNK) signaling pathways, and the Bcl-2 associated X protein (Bax)/B cell lymphoma 2 (Bcl-2) ratio, levels of cleaved caspase-3/9 and cleaved Poly-ADP-ribose polymerase (PARP) were significantly up-regulated following inhibition of ERK1/2 or SAPK/JNK pathways with U0126 or SP600125. After carbonyl cyanide 3-chlorophenylhydrazone (CCCP) treatment, the mitochondrial membrane potential (MMP) of cells was significantly decreased in control group, but stable in the CPSIT_0846 treated one, and less cytochrome c (Cyt.c) was released into the cytoplasm. Inhibition of the ERK1/2 or SAPK/JNK pathway significantly decreased the JC-1 red-green fluorescence signal, and promoted Cyt.c discharge into the cytoplasm in HeLa cells treated with CPSIT_0846. In conclusion, CPSIT_0846 can regulate mitochondrial pathway-mediated apoptosis in HeLa cells by activating the ERK/JNK signaling pathway.

Abstract Arthrogryposis is a group of phenotypically and genetically heterogeneous disorders characterized by congenital contractures of two or more parts of the body; the pathogenesis and the causative genes of arthrogryposis remain undetermined. We examined a four‐generation arthrogryposis pedigree characterized by camptodactyly, limited forearm supination, and loss of myofibers in the forearms and hands. By using whole‐exome sequencing, we confirmed MET p.Y1234C mutation to be responsible for arthrogryposis in this pedigree. MET p.Y1234C mutation caused the failure of activation of MET tyrosine kinase. A Met p.Y1232C mutant mouse model was established. The phenotypes of homozygous mice included embryonic lethality and complete loss of muscles that originated from migratory precursors. Heterozygous mice were born alive and showed reduction of the number of myofibers in both appendicular and axial muscles. Defective migration of muscle progenitor cells and impaired proliferation of secondary myoblasts were proven to be responsible for the skeletal muscle dysplasia of mutant mice. Overall, our study shows MET to be a causative gene of arthrogryposis and MET mutation could cause skeletal muscle dysplasia in human beings.

Aging is a natural and inevitable physiological process that poses a serious threat to physical health, leading to age-related diseases and placing a heavy burden on the public health system. This study explores intervention measures to promote healthy aging and prolong lifespan. Anthocyanins (ACNs), as a class of flavonoids widely presented in fruits, vegetables and grains, exhibit strong antioxidant and anti-inflammatory activities. Recent studies indicate that ACNs exert health effects primarily by interacting with gut microbiota. Here, we introduced the digestion and absorption of ACNs, and mainly elaborated on the role of ACNs in delaying aging through gut microbiota. In addition, we described the changes in gut microbiota mediated by ACNs and their impact on age-related chronic diseases, including cardiovascular diseases, neurodegenerative diseases, cancer, and sarcopenia. Therefore, ACNs have a broad application prospect in the development of functional foods with anti-aging effects by regulating gut microbiota.

Rice is a pivotal cereal crop that provides the staple food for more than half of the world’s population. Along with improvements in the standard of living, people not only pay attention to the grain yield but also to the grain quality. Chalkiness is one of the most important index of grain quality. In this study, qPCG1, a QTL for percentage of chalky grain, was mapped in an interval with a physical distance about 139 kb on chromosome 1 by residual heterozygous line (RHL) method. qPCG1 was incomplete dominant and the additive effect plays a major role and explained 6.8–21.9% of phenotypic variance within the heterogeneous region on chromosome 1. The effect of allele from Zhonghui9308 was decreasing the percentage of chalky grains (PCG). Microscope observation results indicated that there are great differences in the shape, structure and arrangement of starch granule between the chalky part and transparent part. Analysis of starch physicochemical properties showed that the total starch content, amylose content and chain length distribution of amylopectin changed while the protein contents were not apparently affected with the changed chalkiness. qPCG1 had little influence on main agronomic traits and it might be useful in rice breeding for it did not bring negative effect on grain yield while reducing the chalkiness.

The rate of stigma exsertion (SE) is an important trait in rice breeding because the efficiency of hybrid rice seed production can be improved by increasing the percentage of stigmas that exsert. In this study, we developed a near isogenic line (NIL) from two parents, XieqingzaoB (XQZB) and Zhonghoi9308 (ZH9308), which have high and low SE rates in that order. In our previous study, we employed 75 chromosome segment substitution lines (CSSLs) and analyzed quantitative trait loci (QTLs) for their influence on SE rate. The single gene QTL (qSE11), which is located on chromosome 11, was responsible for this trait. In this study, we focused on one of the CSSLs (C65), namely, the NIL (qSE11XB). It contains an introgression segment of XQZB in the genetic background of ZH9308, and exhibits a significantly higher SE rate than that of the parents. We demonstrated that qSE11 regulated both the single and the dual SE rates. They both contribute to the total SE rate. Genetic analysis revealed that qSE11 acted as a single Mendelian factor and that the allele from XQZB increased the SE rate. The validity of our conclusions was established when C65 was used to develop secondary F2 (BC5F2) and F2:3 (BC5F2:3) populations by backcrossing to ZH9308, with subsequent selfing. We entered 3600 plants from the F2 population and 3200 from the F2:3 populations into a genetic dissection program and dissected the major QTL qSE11 to a 350.7-kb region located on chromosome 11. This study will contribute to the future isolation of candidate genes of SE and will play a vital role in future hybrid rice seed production programs.

Lesion mimic mutants are excellent models for research on molecular mechanisms of cell death and defense responses in rice. We identified a new rice lesion mimic mutant lmm24 from a mutant pool of indica rice cultivar “ZhongHui8015”. The LMM24 gene was identified by MutMap, and LMM24 was confirmed as a receptor-like cytoplasmic kinase 109 by amino acid sequence analysis. The lmm24 mutant displayed dark brown lesions in leaves and growth retardation that were not observed in wild-type ZH8015. The results of histochemical staining and TUNEL assays showed enhanced ROS accumulation and cell death in lmm24. Chloroplast degradation was observed in lmm24 leaves, with decreased expression of photosynthesis-related genes and increased expression of the senescence-induced STAYGREEN (SGR) gene and other senescence-associated genes. Furthermore, lmm24 exhibited enhanced resistance to rice blast fungus Magnaporthe oryzae (M. oryzae) and up-regulation of defense response genes. Our data demonstrate that LMM24 regulates cell death and defense responses in rice.