Intra-ovarian inflammatory states and their associations with embryo quality in normal-BMI PCOS patients undergoing IVF treatment.

BACKGROUND: Polycystic ovary syndrome (PCOS) is the main cause of anovulatory infertility in women of reproductive age, and low-grade chronic inflammation plays a key role in the occurrence and development of PCOS. However, obesity, as a likely confounding factor, can affect the inflammatory state of PCOS patients. OBJECTIVE: The aim of this study was to comprehensively investigate intra-ovarian inflammatory states and their impact on embryo quality in PCOS patients with a normal BMI undergoing IVF treatment. METHODS: DIA-mass spectrometry-based proteomics and bioinformatic analysis were combined to comprehensively profile the protein expression of granulosa cells (GCs) from 5 normal-BMI PCOS patients and 5 controls. Thirty-four cytokines were further systematically detected in follicular fluid (FF) from 32 age- and BMI-matched normal-BMI patients using Luminex liquid chip suspension technology. Next, the differentially expressed cytokines were evaluated by enzyme-linked immunosorbent assay (ELISA) in 24 newly recruited subjects, and the relationship between these cytokines and embryo quality in PCOS patients was analysed. Finally, these cytokine levels were compared and evaluated in PCOS patients with different androgen levels. RESULTS: Proteomic analysis showed that the suppression of substance metabolism and steroid biosynthesis, more interestingly, resulted in an enhanced immune and inflammatory response in the GCs of normal-BMI PCOS patients and prompted the involvement of cytokines in this process. Luminex analysis further showed that FF macrophage inflammatory protein-1 beta (MIP-1ß) and stromal cell-derived factor-1 alpha (SDF-1α) levels were significantly increased in normal-BMI PCOS patients compared to controls (P = 0.005; P = 0.035, respectively), and the ELISA results were consistent with these findings. Besides, FF MIP-1ß showed an inverse correlation with the number of D3 good-quality embryos and the good-quality blastocyst rate in patients with PCOS (P = 0.006; P = 0.003, respectively), which remained significant after correction for multiple comparisons. Moreover, SDF-1α levels had no relationship with embryo development in PCOS patients. Additionally, SDF-1α levels were significantly lower in PCOS patients with high androgen levels than in controls (P = 0.031). CONCLUSIONS: Local ovarian inflammation was present in normal-BMI PCOS patients, affecting follicular development, and FF MIP-1ß may be a potential biomarker associated with embryo quality in normal-BMI PCOS patients.

Characterization and fine mapping of a maize lesion mimic mutant (Les8) with enhanced resistance to Curvularia leaf spot and southern leaf blight.

KEY MESSAGE: A novel light-dependent dominant lesion mimic mutant with enhanced multiple disease resistance was physiologically, biochemically, and genetically characterized; the causal gene was fine mapped to a 909 kb interval containing 38 genes. Identification of genes that confer multiple disease resistance (MDR) is crucial for the improvement of maize disease resistance. However, very limited genes are identified as MDR genes in maize. In this study, we characterized a dominant disease lesion mimics 8 (Les8) mutant that had chlorotic lesions on the leaves and showed enhanced resistance to both curvularia leaf spot and southern leaf blight. Major agronomic traits were not obviously altered, while decreased chlorophyll content was observed in the mutant, and the genetic effect of the Les8 mutation was stable in different genetic backgrounds. By BSR-seq analysis and map-based cloning, the LES8 gene was mapped into a 909 kb region containing 38 candidate genes on chromosome 9 wherein no lesion mimic or disease-resistance genes were previously reported. Using transcriptomics analysis, we found that genes involved in defense responses and secondary metabolite biosynthesis were enriched in the significantly up-regulated genes, while genes involved in photosynthesis and carbohydrate-related pathways were enriched in the significantly down-regulated genes in Les8. In addition, there was an overaccumulation of jasmonic acid and lignin but not salicylic acid in Les8. Taken together, this study revealed candidate genes and potential mechanism underlying Les8-conferred MDR in maize.

Underlying mechanism of accelerated cell death and multiple disease resistance in a maize lethal leaf spot 1 allele.

Multiple disease resistance (MDR) in maize has attracted increasing attention. However, the interplay between cell death and metabolite changes and their contributions to MDR remains elusive in maize. In this study, we identified a mutant named as lesion mimic 30 (les30) that showed 'suicidal' lesion formation in the absence of disease and had enhanced resistance to the fungal pathogen Curvularia lunata. Using map-based cloning, we identified the causal gene encoding pheophorbide a oxidase (PAO), which is known to be involved in chlorophyll degradation and MDR, and is encoded by LETHAL LEAF SPOT1 (LLS1). LLS1 was found to be induced by both biotic and abiotic stresses. Transcriptomics analysis showed that genes involved in defense responses and secondary metabolite biosynthesis were mildly activated in leaves of the les30 mutant without lesions, whilst they were strongly activated in leaves with lesions. In addition, in les30 leaves with lesions, there was overaccumulation of defense-associated phytohormones including jasmonic acid and salicylic acid, and of phytoalexins including phenylpropanoids, lignin, and flavonoids, suggesting that their biosynthesis was activated in a lesion-dependent manner. Taken together, our study implies the existence of an interactive amplification loop of interrupted chlorophyll degradation, cell death, expression of defense-related genes, and metabolite changes that results in suicidal lesion formation and MDR, and this has the potential to be exploited by genetic manipulation to improve maize disease resistance.

Tracing haematopoietic stem cell formation at single-cell resolution.

Haematopoietic stem cells (HSCs) are derived early from embryonic precursors, such as haemogenic endothelial cells and pre-haematopoietic stem cells (pre-HSCs), the molecular identity of which still remains elusive. Here we use potent surface markers to capture the nascent pre-HSCs at high purity, as rigorously validated by single-cell-initiated serial transplantation. Then we apply single-cell RNA sequencing to analyse endothelial cells, CD45(-) and CD45(+) pre-HSCs in the aorta-gonad-mesonephros region, and HSCs in fetal liver. Pre-HSCs show unique features in transcriptional machinery, arterial signature, metabolism state, signalling pathway, and transcription factor network. Functionally, activation of mechanistic targets of rapamycin (mTOR) is shown to be indispensable for the emergence of HSCs but not haematopoietic progenitors. Transcriptome data-based functional analysis reveals remarkable heterogeneity in cell-cycle status of pre-HSCs. Finally, the core molecular signature of pre-HSCs is identified. Collectively, our work paves the way for dissection of complex molecular mechanisms regulating stepwise generation of HSCs in vivo, informing future efforts to engineer HSCs for clinical applications.

High-Fat Diets with Differential Fatty Acids Induce Obesity and Perturb Gut Microbiota in Honey Bee.

HFD (high-fat diet) induces obesity and metabolic disorders, which is associated with the alteration in gut microbiota profiles. However, the underlying molecular mechanisms of the processes are poorly understood. In this study, we used the simple model organism honey bee to explore how different amounts and types of dietary fats affect the host metabolism and the gut microbiota. Excess dietary fat, especially palm oil, elicited higher weight gain, lower survival rates, hyperglycemic, and fat accumulation in honey bees. However, microbiota-free honey bees reared on high-fat diets did not significantly change their phenotypes. Different fatty acid compositions in palm and soybean oil altered the lipid profiles of the honey bee body. Remarkably, dietary fats regulated lipid metabolism and immune-related gene expression at the transcriptional level. Gene set enrichment analysis showed that biological processes, including transcription factors, insulin secretion, and Toll and Imd signaling pathways, were significantly different in the gut of bees on different dietary fats. Moreover, a high-fat diet increased the relative abundance of Gilliamella, while the level of Bartonella was significantly decreased in palm oil groups. This study establishes a novel honey bee model of studying the crosstalk between dietary fat, gut microbiota, and host metabolism.

Evolutionary analyses of NIN-like proteins in plants and their roles in nitrate signaling.

Nitrogen (N) is one of the most important essential macro-elements for plant growth and development, and nitrate represents the most abundant inorganic form of N in soils. The nitrate uptake and assimilation processes are finely tuned according to the available nitrate in the surroundings as well as by the internal finely coordinated signaling pathways. The NIN-like proteins (NLPs) harbor both RWP-RK, and Phox and Bem1 (PB1) domains, and they belong to the well-characterized plant-specific RWP-RK transcription factor gene family. NLPs are known to be involved in the nitrate signaling pathway by activating downstream target genes, and thus they are implicated in the primary nitrate response in the nucleus via their RWP-RK domains. The PB1 domain is a ubiquitous protein-protein interaction domain and it comprises another regulatory layer for NLPs via the protein interactions within NLPs or with other essential components. Recently, Ca2+-Ca2+ sensor protein kinase-NLP signaling cascades have been identified and they allow NLPs to have central roles in mediating the nitrate signaling pathway. NLPs play essential roles in many aspects of plant growth and development via the finely tuned nitrate signaling pathway. Furthermore, recent studies have highlighted the emerging roles played by NLPs in the N starvation response, nodule formation in legumes, N and P interactions, and root cap release in higher plants. In this review, we consider recent advances in the identification, evolution, molecular characteristics, and functions of the NLP gene family in plant growth and development.

Novel compound heterozygous mutation in WEE2 is associated with fertilization failure: case report of an infertile woman and literature review.

BACKGROUND: Fertilization failure after intracytoplasmic sperm injection continues to affect couples and the etiology is not well-understood. CASE PRESENTATION: We characterized a couple with 2-year history of primary unexplained infertility. Three different assisted reproduction attempts (IVF + rescue ICSI, ICSI and ICSI-AOA) showed repeated fertilization failure for MII oocyte retrieval after controlled ovarian hyperstimulation. After whole-exome sequencing and sanger sequencing of the couple and their family members, variant pathogenicity was assessed using SIFT, PolyPhen2, Mutation Taster, and Human Splicing Finder software. We identified novel compound heterozygous mutations, c.1535 + 3A > G and c.946C > T (p. Leu316Phe), in WEE2 in the female proband. Trios analysis of the variations revealed an autosomal recessive pattern. c.1535 + 3A > G in WEE2 was predicted to break the wild-type donor site and affect splicing, and the missense mutation c.946C > T (p. Leu316Phe) of WEE2 was predicted to be pathogenic. CONCLUSION: A novel compound heterozygous mutation in WEE2 was identified in an infertile female who experienced repeated fertilization failure even after ICSI-AOA. These novel mutations in WEE2 provided genetic evidence for fertilization failure.

ATF4 plays a pivotal role in the development of functional hematopoietic stem cells in mouse fetal liver.

The fetal liver (FL) serves as a predominant site for expansion of functional hematopoietic stem cells (HSCs) during mouse embryogenesis. However, the mechanisms for HSC development in FL remain poorly understood. In this study, we demonstrate that deletion of activating transcription factor 4 (ATF4) significantly impaired hematopoietic development and reduced HSC self-renewal in FL. In contrast, generation of the first HSC population in the aorta-gonad-mesonephros region was not affected. The migration activity of ATF4(-/-) HSCs was moderately reduced. Interestingly, the HSC-supporting ability of both endothelial and stromal cells in FL was significantly compromised in the absence of ATF4. Gene profiling using RNA-seq revealed downregulated expression of a panel of cytokines in ATF4(-/-) stromal cells, including angiopoietin-like protein 3 (Angptl3) and vascular endothelial growth factor A (VEGFA). Addition of Angptl3, but not VEGFA, partially rescued the repopulating defect of ATF4(-/-) HSCs in the culture. Furthermore, chromatin immunoprecipitation assay in conjunction with silencing RNA-mediated silencing and complementary DNA overexpression showed transcriptional control of Angptl3 by ATF4. To summarize, ATF4 plays a pivotal role in functional expansion and repopulating efficiency of HSCs in developing FL, and it acts through upregulating transcription of cytokines such as Angptl3 in the microenvironment.

A RNA-Seq Analysis of the Response of Photosynthetic System to Low Nitrogen Supply in Maize Leaf.

Nitrogen is a major limiting factor for crop productivity. The relationship between photosynthesis and nitrogen nutrition has been widely studied. However, the molecular response of leaf photosynthesis to low nitrogen supply in crops is less clear. In this study, RNA sequencing technology (RNA-Seq) was used to investigate the gene expressions related to photosynthesis in maize in response to low nitrogen supply. It was found that low nitrogen supply down-regulated the expression of genes involved in photosystem I (PSI) and photosystem II (PSII). Thus, low nitrogen supply down-regulated the expression of genes related to the antenna system, reduced light absorption, light transport, and electron transport. Correspondingly, the parameters related to chlorophyll fluorescence were very sensitive to nitrogen deficiency. Under low nitrogen supply, leaf chlorophyll content, actual quantum yield of PSII photochemistry, photochemical quenching, and electron transport rate, were reduced. However, the thermal diffusion and chlorophyll fluorescence were increased. RNA-Seq was used to analyze the genes involved in the response of leaf photosynthesis to low nitrogen supply in maize. These results highlight the possibility of utilizing chlorophyll fluorescence parameters, and the related genes, as indicators for plant nitrogen nutrition. This could lead to the development of new tools to make precise nitrogen fertilizer recommendations and select nitrogen-efficient genotypes.

[CatSper in sperm hyperactivation and male infertility: Advances in studies].

The CatSper channel is known as one of the most important Ca²âº channels on the cell membrane of mammalian sperm and plays a key role in the motility, hyperactivation and fertilization function of sperm. The CatSper protein, expressed exclusively in the principal piece of the sperm tail, is composed of CatSper1-4 and 5 auxiliary unitsß,γ,δ and ε, and has an essential part in the functional and structural domains of Ca²âºas well as in the spatiotemporal regulation of the P-Tyr protein, sperm hyperactivation, efficient sperm migration in the oviduct, egg penetration, and normal fertility. Recent studies show that functional deficiency of CatSper seriously affects sperm function,and the loss of any one of its 9 subunits may lead to male reproductive dysfunction. This paper outlines recent advances in the studies of the CatSperprotein, focusing on its expression, location, structure, and regulation,as well as itsinfluence on sperm hyperactivation and male reproduction.

Antibiotic exposure alters the honeybee gut microbiota and may interfere with the honeybee behavioral caste transition.

Behavioral division is essential for the sustainability and reproduction of honeybee populations. While accumulating evidence has documented that antibiotic exposure interferes with bee behavioral divisions, how the gut microbiome, host physiology, and genetic regulation are implicated in this process remains understudied. Here, by constructing single-cohort colonies, we validated that the gut microbiota varied in composition between age-matched nurse and forager bees. Perturbing the gut microbiota with a low dose of antibiotic retained the gut bacterial size, but the structure of the microbial community continuously diverged from the control group after antibiotic treatment. Fewer foragers were observed in the antibiotic groups in the field experiment. A combinatorial effect of decreased gut metabolic gene repertoires, reduced brain neurotransmitter titers, and downregulated brain immune genes could potentially be related to behavioral tasks transition delay. This work indicates that the disturbance to both the gut microbiome and host physiologies after antibiotic exposure may have implications on social behavior development, highlighting the need for further research focusing on antibiotic pollution threatening the honeybee population's health.

Spatial accumulation of lignin monomers and cellulose underlying stalk strength in maize.

Lodging largely affects yield, quality and mechanical harvesting of maize. Stalk strength is one of the major factors that affect maize lodging. Although plant cell wall components including lignin and cellulose were known to be associated with stalk strength and lodging resistance, spatial accumulation of specific lignin monomers and cellulose in different tissues and their association with stalk strength in maize was not clearly understood. In this study, we found that both G and S lignin monomers accumulate highest in root, stem rind and leaf vein. Consistently, most lignin biosynthetic genes were expressed higher in root and stem than in other tissues. However, cellulose appears to be lowest in root. There are only mild changes of G lignin and cellulose in different internodes. Instead, we noticed a dramatic decrease of S-lignin accumulation and lignin biosynthetic gene expression in 2nd to 4th internodes wherein stem breakage usually occurs, thereby revealing a few candidate lignin biosynthetic genes associated with stalk strength. Moreover, stalk strength is positively correlated with G, S lignin, and cellulose, but negatively correlated with S/G ratio based on data of maize lines with high or low stalk strength. Loss-of-function of a caffeic acid o-methyltransferase (COMT), which is involved in S lignin biosynthesis, in the maize bm3 mutant, leads to lower stalk strength. Our data collectively suggest that stalk strength is determined by tissue-specific accumulation of lignin monomers and cellulose, and manipulation of the cell wall components by genetic engineering is vital to improve maize stalk strength and lodging resistance.

Copine proteins are required for brassinosteroid signaling in maize and Arabidopsis.

Copine proteins are highly conserved and ubiquitously found in eukaryotes, and their indispensable roles in different species were proposed. However, their exact function remains unclear. The phytohormone brassinosteroids (BRs) play vital roles in plant growth, development and environmental responses. A key event in effective BR signaling is the formation of functional BRI1-SERK receptor complex and subsequent transphosphorylation upon ligand binding. Here, we demonstrate that BONZAI (BON) proteins, which are plasma membrane-associated copine proteins, are critical components of BR signaling in both the monocot maize and the dicot Arabidopsis. Biochemical and molecular analyses reveal that BON proteins directly interact with SERK kinases, thereby ensuring effective BRI1-SERK interaction and transphosphorylation. This study advances the knowledge on BR signaling and provides an important target for optimizing valuable agronomic traits, it also opens a way to study steroid hormone signaling and copine proteins of eukaryotes in a broader perspective.

Distinct Roles of Honeybee Gut Bacteria on Host Metabolism and Neurological Processes.

The honeybee possesses a limited number of bacterial phylotypes that play essential roles in host metabolism, hormonal signaling, and feeding behavior. However, the contribution of individual gut members in shaping honeybee brain profiles remains unclear. By generating gnotobiotic bees which were mono-colonized by a single gut bacterium, we revealed that different species regulated specific modules of metabolites in the hemolymph. Circulating metabolites involved in carbohydrate and glycerophospholipid metabolism pathways were mostly regulated by Gilliamella, while Lactobacillus Firm4 and Firm5 mainly altered amino acid metabolism pathways. We then analyzed the brain transcriptomes of bees mono-colonized with these three bacteria. These showed distinctive gene expression profiles, and genes related to olfactory functions and labor division were upregulated by Lactobacillus. Interestingly, differentially spliced genes in the brains of gnotobiotic bees largely overlapped with those of bees unresponsive to social stimuli. The differentially spliced genes were enriched in pathways involved in neural development and synaptic transmission. We showed that gut bacteria altered neurotransmitter levels in the brain. In particular, dopamine and serotonin, which show inhibitory effects on the sensory sensitivity of bees, were downregulated in bacteria-colonized bees. The proboscis extension response showed that a normal gut microbiota is essential for the taste-related behavior of honeybees, suggesting the contribution of potential interactions among different gut species to the host's physiology. Our findings provide fundamental insights into the diverse functions of gut bacteria which likely contribute to honeybee neurological processes. IMPORTANCE The honeybee possesses a simple and host-restricted gut community that contributes to the metabolic health of its host, while the effects of bacterial symbionts on host neural functions remain elusive. We found that the colonization of specific bee gut bacteria regulates distinct circulating metabolites enriched in carbohydrate, amino acid, and glycerophospholipid metabolic pathways. The brains of bees colonized with different gut members display distinct transcriptomic profiles of genes crucial for bee behaviors and division of labor. Alternative splicing of genes related to disordered bee behaviors is also mediated. The presence of gut bacteria promotes sucrose sensitivity with major neurotransmitters being regulated in the brain. Our findings demonstrate how individual bee gut species affect host behaviors, highlighting the gut-brain connections important for honeybee neurobiological and physiological states.

Honeybee gut Lactobacillus modulates host learning and memory behaviors via regulating tryptophan metabolism.

Honeybees are highly social insects with a rich behavioral repertoire and are a versatile model for neurobiological research. Their gut microbiota comprises a limited number of host-restricted bacterial phylotypes that are important for honeybee health. However, it remains unclear how specific gut members affect honeybee behaviors. Here, we find that antibiotic exposure disturbs the gut community and influences honeybee phenotypes under field conditions. Using laboratory-generated gnotobiotic bees, we show that a normal gut microbiota is required for olfactory learning and memory abilities. Brain transcriptomic profiling reveals distinct brain gene expression patterns between microbiota-free and conventional bees. Subsequent metabolomic analyses of both hemolymph and gut samples show that the microbiota mainly regulates tryptophan metabolism. Our results indicate that host-specific Lactobacillus strains promote memory behavior by transforming tryptophan to indole derivatives that activate the host aryl hydrocarbon receptor. Our findings highlight the contributions of specific gut members to honeybee neurological processes, thus providing a promising model to understand host-microbe interactions.

Comparative Transcriptome Analysis Reveals Common and Developmental Stage-Specific Genes That Respond to Low Nitrogen in Maize Leaves.

A growing leaf can be divided into three sections: division zone, elongation zone, and maturation zone. In previous studies, low nitrogen (LN) inhibited maize growth and development, especially leaf growth; however, the gene expression in response to LN in different regions in leaf were not clear. Here, using hydroponics and a transcriptome approach, we systematically analyzed the molecular responses of those zones and differentially expressed genes (DEG) in response to LN supply. Developmental stage-specific genes (SGs) were highly stage-specific and involved in distinct biological processes. SGs from division (SGs-DZ) and elongation zones (SGs-EZ) were more related to developmentally dependent processes, whereas SGs of the maturation zone (SGs-MZ) were more related to metabolic processes. The common genes (CGs) were overrepresented in carbon and N metabolism, suggesting that rebalancing carbon and N metabolism in maize leaves under LN condition was independent of developmental stage. Coexpression modules (CMs) were also constructed in our experiment and a total of eight CMs were detected. Most of SGs-DZ and SGs-EZ were classified into a set termed CM turquoise, which was mainly enriched in ribosome and DNA replication, whereas several genes from SGs-MZ and CGs were clustered into CM blue, which mainly focused on photosynthesis and carbon metabolism. Finally, a comprehensive coexpression network was extracted from CM blue, and several maize CONSTANS-LIKE(ZmCOL) genes seemed to participate in regulating photosynthesis in maize leaves under LN condition in a developmental stage-specific manner. With this study, we uncovered the LN-responsive CGs and SGs that are important for promoting plant growth and development under insufficient nitrogen supply.

Geographical resistome profiling in the honeybee microbiome reveals resistance gene transfer conferred by mobilizable plasmids.

BACKGROUND: The spread of antibiotic resistance genes (ARGs) has been of global concern as one of the greatest environmental threats. The gut microbiome of animals has been found to be a large reservoir of ARGs, which is also an indicator of the environmental antibiotic spectrum. The conserved microbiota makes the honeybee a tractable and confined ecosystem for studying the maintenance and transfer of ARGs across gut bacteria. Although it has been found that honeybee gut bacteria harbor diverse sets of ARGs, the influences of environmental variables and the mechanism driving their distribution remain unclear. RESULTS: We characterized the gut resistome of two closely related honeybee species, Apis cerana and Apis mellifera, domesticated in 14 geographic locations across China. The composition of the ARGs was more associated with host species rather than with geographical distribution, and A. mellifera had a higher content of ARGs in the gut. There was a moderate geographic pattern of resistome distribution, and several core ARG groups were found to be prevalent among A. cerana samples. These shared genes were mainly carried by the honeybee-specific gut members Gilliamella and Snodgrassella. Transferrable ARGs were frequently detected in honeybee guts, and the load was much higher in A. mellifera samples. Genomic loci of the bee gut symbionts containing a streptomycin resistance gene cluster were nearly identical to those of the broad-host-range IncQ plasmid, a proficient DNA delivery system in the environment. By in vitro conjugation experiments, we confirmed that the mobilizable plasmids could be transferred between honeybee gut symbionts by conjugation. Moreover, "satellite plasmids" with fragmented genes were identified in the integrated regions of different symbionts from multiple areas. CONCLUSIONS: Our study illustrates that the gut microbiota of different honeybee hosts varied in their antibiotic resistance structure, highlighting the role of the bee microbiome as a potential bioindicator and disseminator of antibiotic resistance. The difference in domestication history is highly influential in the structuring of the bee gut resistome. Notably, the evolution of plasmid-mediated antibiotic resistance is likely to promote the probability of its persistence and dissemination. Video Abstract.

The physiological response of photosynthesis to nitrogen deficiency.

Nitrogen (N), as a macro-element, plays a vital role in plant growth and development. N deficiency affects plant productivity by decreasing photosynthesis, leaf area and longevity of green leaf. To date, many studies have reported that the relationship between photosynthesis and N supply. Here, we summarized the physiological response of photosynthesis to N deficiency in leaf structure and N allocation within the leaf. In serious N stress, photosynthetic rate decreases for almost all plants. The reasons as follows:(1) reducing stomatal conductance of mesophyll cell (gs) and bundle sheath cells (gbs) which influences intercellular CO2 concentration; (2) reducing the content of bioenergetics and light-harvesting protein which inhibits electron transport rate and increase the light energy dissipated as heat; (3) reducing the content and/or activity of photosynthetic enzymes which reduces carboxylation rate. During reproductive stage, N stress induces plant senescence and N components degradation, especially photosynthetic enzymes and thylakoid N, and thus reduces photosynthesis. To keep high grain yield in low N deficiency, we should choose the genotype with higher N allocation within bioenergetics and lower degradation of photosynthetic enzymes. This review provides a generalized N allocation in response to N stress and gives a new prospect for breeding N-efficient genotypes.

Honey bee genetics shape the strain-level structure of gut microbiota in social transmission.

BACKGROUND: Honey bee gut microbiota transmitted via social interactions are beneficial to the host health. Although the microbial community is relatively stable, individual variations and high strain-level diversity have been detected across honey bees. Although the bee gut microbiota structure is influenced by environmental factors, the heritability of the gut members and the contribution of the host genetics remains elusive. Considering bees within a colony are not readily genetically identical due to the polyandry of the queen, we hypothesize that the microbiota structure can be shaped by host genetics. RESULTS: We used shotgun metagenomics to simultaneously profile the microbiota and host genotypes of bees from hives of four different subspecies. Gut composition is more distant between genetically different bees at both phylotype- and "sequence-discrete population" levels. We then performed a successive passaging experiment within colonies of hybrid bees generated by artificial insemination, which revealed that the microbial composition dramatically shifts across batches of bees during the social transmission. Specifically, different strains from the phylotype of Snodgrassella alvi are preferentially selected by genetically varied hosts, and strains from different hosts show a remarkably biased distribution of single-nucleotide polymorphism in the Type IV pili loci. Genome-wide association analysis identified that the relative abundance of a cluster of Bifidobacterium strains is associated with the host glutamate receptor gene specifically expressed in the bee brain. Finally, mono-colonization of Bifidobacterium with a specific polysaccharide utilization locus impacts the alternative splicing of the gluR-B gene, which is associated with an increased GABA level in the brain. CONCLUSIONS: Our results indicated that host genetics influence the bee gut composition and suggest a gut-brain connection implicated in the gut bacterial strain preference. Honey bees have been used extensively as a model organism for social behaviors, genetics, and the gut microbiome. Further identification of host genetic function as a shaping force of microbial structure will advance our understanding of the host-microbe interactions. Video abstract.

Commonly and Specifically Activated Defense Responses in Maize Disease Lesion Mimic Mutants Revealed by Integrated Transcriptomics and Metabolomics Analysis.

Disease lesion mimic (Les/les) mutants display disease-like spontaneous lesions in the absence of pathogen infection, implying the constitutive activation of defense responses. However, the genetic and biochemical bases underlying the activated defense responses in those mutants remain largely unknown. Here, we performed integrated transcriptomics and metabolomics analysis on three typical maize Les mutants Les4, Les10, and Les17 with large, medium, and small lesion size, respectively, thereby dissecting the activated defense responses at the transcriptional and metabolomic level. A total of 1,714, 4,887, and 1,625 differentially expressed genes (DEGs) were identified in Les4, Les10, and Les17, respectively. Among them, 570, 3,299, and 447 specific differentially expressed genes (SGs) were identified, implying a specific function of each LES gene. In addition, 480 common differentially expressed genes (CGs) and 42 common differentially accumulated metabolites (CMs) were identified in all Les mutants, suggesting the robust activation of shared signaling pathways. Intriguingly, substantial analysis of the CGs indicated that genes involved in the programmed cell death, defense responses, and phenylpropanoid and terpenoid biosynthesis were most commonly activated. Genes involved in photosynthetic biosynthesis, however, were generally repressed. Consistently, the dominant CMs identified were phenylpropanoids and flavonoids. In particular, lignin, the phenylpropanoid-based polymer, was significantly increased in all three mutants. These data collectively imply that transcriptional activation of defense-related gene expression; increase of phenylpropanoid, lignin, flavonoid, and terpenoid biosynthesis; and inhibition of photosynthesis are generalnatures associated with the lesion formation and constitutively activated defense responses in those mutants. Further studies on the identified SGs and CGs will shed new light on the function of each LES gene as well as the regulatory network of defense responses in maize.