Effects of Simulated Acid Rain on Photosynthesis in Pinus massoniana and Cunninghamia lanceolata in Terms of Prompt Fluorescence, Delayed Fluorescence, and Modulated Reflection at 820 nm.

The effects of simulated acid rain (SAR) on the photosynthetic performance of subtropical coniferous species have not been thoroughly investigated. In this study, we treated two coniferous species, Pinus massoniana (PM) and Cunninghamia lanceolata (CL), with four gradients of SAR and then analyzed their photosynthetic activities through measurements of gas exchange, prompt fluorescence (PF), delayed fluorescence (DF), and modulated reflection at 820 nm (MR820). Gas exchange analysis indicated that the decrease in the net photosynthetic rate (Pn) in PM and CL was unrelated to stomatal factors. For the PF transients, SAR induced positive K-band and L-band, a significant reduction in photosynthetic performance index (PIABS), the quantum yield of electron transfer per unit cross-section (ETO/CSm), and maximal photochemical efficiency of photosystem II (Fv/Fm). Analysis of the MR820 kinetics showed that the re-reduction kinetics of PSI reaction center (P700+) and plastocyanin (PC+) became slower and occurred at later times under SAR treatment. For the DF signals, a decrease in the amplitude of the DF induction curve reduced the maximum value of DF (I1). These results suggested that SAR obstructed photosystem II (PSII) donor-side and acceptor-side electron transfer capacity, impaired the connectivity between PSII and PSI, and destroyed the oxygen-evolving complex (OEC). However, PM was better able to withstand SAR stress than CL, likely because of the activation of a protective mechanism.

The status and risk factors for anxiety/depression in patients with atrophic chronic gastritis: a cross-sectional study.

BACKGROUND: Atrophic chronic gastritis (ACG) is a preneoplastic condition of gastric carcinoma. Numerous studies have shown anxiety and depression can affect gastrointestinal function, which may promote gastrointestinal disorders development and progression. Thus, we hypothesized that anxiety and depression may enhance the development and progression of ACG. In this study, we aimed to analyse risk factors for anxiety and depression in ACG patients and integrate these risk factors to construct an effective clinical prediction model. METHODS: In total, 118 ACG patients were included from July 2021 to May 2022. Anxiety and depression were assessed utilizing the Generalized Anxiety Disorder-7 (GAD-7) and Patient Health Questionnaire-9 (PHQ-9). Data were collected on demographic characteristics, lifestyle, and dietary habits. Risk factors for anxiety and depression were explored with univariate analysis and multivariate stepwise logistic regression, and risk prediction models were built. RESULTS: Among 118 ACG patients, 36.4% had anxiety, 25.4% had depression, and 21.2% had both anxiety and depression. Poor sleep quality [odd ratio (OR) 4.32, 95% confidence interval (CI): 1.60-11.65, P=0.004] was positively associated with risk of anxiety, while smoking (OR 0.15, 95% CI: 0.03-0.68, P=0.014) and weekly exercise time (OR 0.89, 95% CI: 0.79-0.99, P=0.037) were negatively associated with risk of anxiety. The area under the receiver operating characteristic (ROC) curve was 80.3%, 95% CI: [0.722-0.885]. The sensitivity was 72.1%, and the specificity was 78.7%. Poor sleep quality (P<0.001, OR 23.89, 95% CI: 4.05-141.05), high salt diet (P=0.004, OR 6.94, 95% CI: 1.86-25.96), family history of tumours (P=0.020, OR 6.10, 95% CI: 1.33-27.93), and abdominal pain (P=0.018, OR 4.44, 95% CI: 1.29-15.23) were positively associated with the risk of depression, with an area under the ROC curve of 77.3%, 95% CI: 0.687-0.860. The sensitivity was 83.3%, and the specificity was 62.5%. CONCLUSIONS: Potential anxiety and depression in ACG patients can be identified early by referring to risk factors and protective factors. The prediction model could be used to detect anxiety and depression in ACG patients at their earliest stage and provide meaningful suggestions for ACG patients.

Telomere is shortened in patients with irritable bowel syndrome in the Chinese population.

BACKGROUND AND AIM: Telomere shortening is an accepted indicator of aging. Many studies have investigated an association between leukocyte telomere length (LTL) and psychiatric disorders. Mental or psychological factors could be an important cause of irritable bowel syndrome (IBS). However, there are currently few research evaluating correlations between LTL and IBS. METHODS: We examined associations between LTL and IBS using quantitative polymerase chain reaction in independent cohorts, including 205 patients with IBS and 189 healthy controls. Furthermore, we examined whether mental or psychological factors, types of IBS, duration of IBS and antidepressants had an association with LTL in patients with IBS. RESULTS: Among total samples, patients with IBS presented shorter LTL when compared to healthy controls (P < 0.0001). Moreover, in subgroup analyses of patients with IBS, not only the LTL in patients with IBS caused by mental or psychological factors was shorter (P < 0.0001), but also in patients with IBS that were caused by other factors (P = 0.0082). Furthermore, LTL in patients with IBS who had taken antidepressants for more than 1 month was longer than that in patients with IBS who did not take antidepressants or took for less than 1 month (P < 0.0001). CONCLUSIONS: This is the first study to describe the relationship between LTL and IBS. This study showed significantly shorter telomeres in patients with IBS. Our findings suggest that LTL may hold the potential to serve as a predictor of IBS diagnosis.

Allometry and Yield Stability of Cereals.

Crop plants grow, and then, they allocate resources to different structures, including seeds and fruits, which represent yield in most crops. We define the yield stability of a genotype as its ability to reduce the effects of temporal variation in resources and conditions on yield production, and we argue that yield stability can be understood in terms of two processes: (1) crop survival and growth (biomass production): the ability of the crop plants to survive and produce biomass under the range of conditions to which it is exposed and (2) the pattern of allocation of this biomass to yield across this range of conditions. Plant breeders and crop physiologists have focused on (1), but much less attention has been paid to (2). We hypothesize that (2) is primarily the result of reproductive allometry: the quantitative relationship between vegetative and reproductive biomass. Ecological theory and the allometric models we present predict a tradeoff between (a) the ability of a genotype to produce yield over a wide variety of conditions and (b) its ability to produce very high yields under optimal or near-optimal conditions. We reanalyze the data from two recent studies, and the results are consistent with this hypothesis. Yield stability in crops corresponds to bet-hedging in evolutionary ecological theory. It is the most appropriate strategy for smallholder farmers in developing countries, a group that comprises most of the farmers in the world. Researchers and crop breeders need to rethink their objectives if they want to develop optimal varieties for these farmers.

Unconjugated Bilirubin Attenuates DSS-Induced Colitis Potentially via Enhancement of Bilirubin Reabsorption.

Studies increasingly show that ulcerative colitis (UC) is a consequence of an imbalance between oxidative stress and antioxidant capacity. Bilirubin exerts an anti-inflammatory effect by scavenging reactive oxygen species (ROS), although the exact mechanism is not completely understood. The aim of this study was to determine the role of serum bilirubin in UC using patient data and a mouse model of dextran sodium sulfate (DSS)-induced colitis. We found that low levels of serum bilirubin correlated to a higher risk of UC in a retrospective case-control population. Pre-treatment with exogenous unconjugated bilirubin (UCB) significantly enhanced colonic bilirubin absorption in mice, and attenuated the DSS-induced body weight loss, colon shortening and histopathological damage. Mechanistically, bilirubin prevented the infiltration of inflammatory cells, and decreased the levels of myeloperoxidase and pro-inflammatory cytokines in the serum and colon. Moreover, bilirubin inhibited ROS and malondialdehyde production, scavenged superoxide anions (O2 ·-) from the colon and enhanced the total antioxidant capacity. In conclusion, exogenous UCB attenuated DSS-induced colitis by directly scavenging O2 ·- and enhancing bilirubin reabsorption in the colon via enterohepatic cycling.

A Color Restoration Algorithm for Diffractive Optical Images of Membrane Camera.

In order to verify the technology of the membrane diffractive imaging system for Chinese next generation geo-stationary earth orbit (GEO) satellite, a series of ground experiments have been carried out using a membrane optical camera with 80 mm aperture (Φ80) lens. The inherent chromatic aberration due to diffractive imaging appears in the obtained data. To address the issue, an effective color restoration algorithm framework by matching, tailoring, and non-linearly stretching the image histograms is proposed in this letter. Experimental results show the proposed approach has good performances in color restoration of the diffractive optical images than previous methods. The effectiveness and robustness of the algorithm are also quantitatively assessed using various color deviation indexes. The results indicate that the chromatic aberration of diffractive images can be effectively removed by about 85%. Also, the proposed method presents reasonable computational efficiency.

The effect of different combinations of antibiotic cocktails on mice and selection of animal models for further microbiota research.

The gut microbiota is closely related to host health and disease. However, there are no suitable animal models available at present for exploring its functions. We analyzed the effect of 3 different antibiotic cocktails (ABx) via two administration routes on the composition of murine gut microbiota, as well as on the general physiological and metabolic indices. High-throughput 16S rRNA sequencing showed that ABx treatment altered the gut microbiota community structure, and also caused low-degree inflammation in the colon. In addition, ad libitum administration of antibiotics depleted the gut microbiota more effectively compared to direct oral gavage, especially with 3ABx. The ABx treatment also had a significant impact on renal and liver functions, as indicated by the altered serum levels of creatinine, urea, total triglycerides, and total cholesterol. Finally, Spearman's correlation analysis showed that the predominant bacterial genera resulting from ABx intervention, including Lactobacillus, Roseburia, and Candidatus-Saccharimonas, were negatively correlated with renal function indices. Taken together, different antibiotic combinations and interventions deplete the gut microbiota and induce physiological changes in the host. Our findings provide the basis for developing an adaptive animal model for studying gut microbiota. KEY POINTS: • Ad libitum administration of 3ABx can effectively deplete intestinal microbiota. • ABx treatment may have slight effect on renal and liver function. • The levels of urea and creatinine correlated with the growth of Roseburia.

Inhibition of PD-1 Protects against TNBS-Induced Colitis via Alteration of Enteric Microbiota.

METHODS: Colitis was induced in mice using 2,4,6-trinitrobenzene-sulfonic acid (TNBS), and mice were subsequently treated with either a PD-1 inhibitor or 5-amino-salicylic acid (ASA) as a positive control. Body weight, disease activity index (DAI), colon length, and tissue damage were evaluated, and the enteric microbiota was profiled using high-throughput 16S rRNA sequencing of fecal samples from the experimental mice. RESULTS: TNBS caused mice to experience IBD-like symptoms, which were attenuated by the PD-1 inhibitor, as indicated by a decrease in DAI scores (p = 0.0002). Furthermore, in this mouse model of IBD, PD-1 inhibition improved the alpha diversity as well as restored the beta diversity of the enteric microbiome. It also significantly enriched the abundance of short-chain fatty acid- (SCFA-) producing bacteria of the Firmicutes (p < 0.05) and Bacteroidetes (p < 0.05) phyla but depopulated Proteobacteria (p < 0.05). CONCLUSION: PD-1 inhibition can partly mitigate TNBS-induced colitis and restore the enteric microbiota by enriching the abundance of SCFA-producing bacteria.

Protein expression-based classification of gastric cancer by immunohistochemistry of tissue microarray.

Recently, the Cancer Genome Atlas and Asian Cancer Research Group propose two new classifications system of gastric cancer by using multi-platforms of molecular analyses. However, these highly complicated and cost technologies have not yet been translated into full clinical utility. In addition, the clinicians are expected to gain more guidance of treatment for different molecular subtypes. In this study, we developed a panel of gastric cancer patients in population from Southern China using commercially accessible TMA and immunohistochemical technology. A cohort of 259 GC patients was classified into 4 subtypes on the basis of expression of mismatch repair proteins (PMS2, MLH1, MSH2, and MSH6), E-cadherin and p21 protein. We observed that the subtypes presented distinct prognosis. dMMR-like subtype was associated with the best prognosis, and E-cadherin-a subtype was associated with the worst prognosis. Patients with p21-High and p21-Ligh subtypes had intermediate overall survival. In multivariate analysis, the dMMR-like subtype remained an independent prediction power for overall survival in the model. We described a molecular classification of gastric cancers using clinically applicable assay. The biological relevance of the four subtypes was illustrated by significant differences in prognosis. Our molecular classification provided an effective and inexpensive screening tool for improving prognostic models. Nevertheless, our study should be considered preliminary and carries a limited predictive value as a single-center retrospective study.

Prodigiosin impairs autophagosome-lysosome fusion that sensitizes colorectal cancer cells to 5-fluorouracil-induced cell death.

Chemotherapy failure is a major cause of recurrence and poor prognosis in colorectal cancer (CRC) patients. Inhibition of autophagy is a promising strategy to augment the cytotoxicity of chemotherapeutic agents. We identified prodigiosin, a secondary metabolite produced by various bacteria, as a novel autophagy inhibitor that interfered with the autophagic flux in CRC cells by blocking autophagosome-lysosome fusion and lysosomal cathepsin maturation, resulting in the accumulation of LC3B-II and SQSTM. Suppression of autophagy by prodigiosin sensitized the CRC cells to 5-fluorouracil (5-Fu) in vitro, and the combination treatment markedly reduced cancer cell viability partly via caspase-dependent apoptosis. Furthermore, prodigiosin and 5-Fu synergistically inhibited CRC xenograft growth in vivo without any adverse effects. In conclusion, prodigiosin inhibits late stage autophagy and sensitizes tumor cells to 5-Fu, indicating its therapeutic potential in CRC.

Association of DCBLD2 upregulation with tumor progression and poor survival in colorectal cancer.

PURPOSE: DCBLD2 expression dysregulation has been reported in several types of human cancer. As yet, however, the role of DCBLD2 in colorectal cancer (CRC) is not known. METHODS: CRC tissues were obtained from patients undergoing surgery from February 2009 to May 2014 (n = 90). Tissue microarray construction and immunohistochemistry were carried out to determine DCBLD2 expression. In vivo studies were performed in 4-week-old BALB/c nude mice. In vitro studies were conducted using CRC-derived HT29 and HCT116 cell lines. RESULTS: DCBLD2 expression was found to be significantly increased in CRC tissues compared to adjacent normal tissues (p < 0.001). In addition, we found that DCBLD2 expression was positively correlated with the stage of the disease, the degree of differentiation and vascular invasion. High DCBLD2 expression was significantly associated with a poor overall survival. In vitro, DCBLD2 expression downregulation significantly reduced CRC cell proliferation and invasion. In a mouse xenograft model, DCBLD2 expression downregulation reduced lung metastasis and increased overall survival. Gene set enrichment analysis (GSEA) revealed that DCBLD2 overexpression induces epithelial-mesenchymal transition (EMT) and activates the JAK/STAT3 pathway. CONCLUSIONS: We found that high DCBLD2 expression correlated with a poor clinical outcome, as well as tumorigenesis, invasion and metastasis of CRC cells. DCBLD2 may serve as a prognostic biomarker and a novel therapeutic target for CRC.

LncRNA CR749391 acts as a tumor suppressor to upregulate KLF6 expression via interacting with miR-181a in gastric cancer.

Long non-coding RNAs (lncRNAs) are novel regulators for post-transcriptional gene expression, and altered lncRNAs function and expression are associated with tumorigenesis and cancer progression, although the biological functions of most lncRNAs in various cancer types and their underlying regulatory interactions have remained largely elusive. Our previous study identified microRNA (miR)-181a as a regulator of Kruppel-like factor 6 (KLF6). In the present study, a bioinformatical analysis was performed to identify the novel lncRNA CR749391 as a potential regulator of miR-181a that contains four putative binding sites. Subsequent in vitro experiments in gastric cancer (GC) cells demonstrated that CR749391 interacted with miR-181a to regulate KLF6 expression. First, a direct binding interaction was confirmed using luciferase reporter and RNA immunoprecipitation and pull-down assays. In addition, CR749391 was observed to be downregulated in GC compared with that of normal gastric cell lines. A functional study also revealed that CR749391 depletion in normal gastric epithelial cells promoted cell viability, migration and invasion, and conferred resistance to apoptosis, whereas ectopic CR749391 overexpression had the opposite effect in GC cells and inhibited in vivo tumor growth. In addition, CR749391 was observed to be downregulated in GC compared with that of normal gastric tissues, which was associated with KLF6 but inversely associated with miR-181a levels. Overall, the CR749391/miR-181a regulatory interaction and association between CR749391 and KLF6 may enhance the current understanding of GC pathogenesis, although CR749391 association with GC prognosis needs further study. The current study could provide a novel approach for lncRNA-mediated targeted GC therapy.

Are There Potential Applications of Fecal Microbiota Transplantation beyond Intestinal Disorders?

Intestinal microbial dysbiosis is associated with various intestinal and extraintestinal disorders. Fecal microbiota transplantation (FMT), a type of fecal bacteriotherapy, is considered an effective therapeutic option for recurrent Clostridium difficile infection (rCDI) and also has important value in other intestinal diseases including irritable bowel syndrome (IBS) and inflammatory bowel disease (IBD). The purpose of this review is to discuss promising therapeutic value in extraintestinal diseases associated with gut microbial dysbiosis, including liver, metabolic, chronic kidney, neuropsychiatric, allergic, autoimmune, and hematological diseases as well as tumors.

RARß acts as both an upstream regulator and downstream effector of miR-22, which epigenetically regulates NUR77 to induce apoptosis of colon cancer cells.

This study investigates the mechanism and consequences of microRNA-22 ( miR-22) induction. Our data revealed for the first time that retinoic acid (RA) and histone deacetylase (HDAC) inhibitors, including short-chain fatty acids and suberanilohydroxamic acid (SAHA), could individually or in combination induce miR-22. This induction was mediated via RA receptor ß (RARß) binding to a direct repeat 5 (DR5) motif. In addition, we uncovered HDAC1 as a novel miR-22 target. In an miR-22-dependent manner, HDAC inhibitors and RA reduced HDAC1, HDAC4, and sirtuin 1 (SIRT1), which were involved in chromatin remodeling of the RARß and nerve growth factor IB ( NUR77). Thus, HDAC inhibitors and RA-induced miR-22 resulted in simultaneous induction of cytoplasmic RARß and NUR77, leading to apoptosis of colon cancer cells. In mice, miR-22 and its inducers inhibited the growth of xenograft colon cancer. Moreover, tumor size reduction was accompanied by elevated miR-22, NUR77, and RARß and by reduced HDACs. In human colon polyps and adenocarcinomas, miR-22 and RARß were consistently reduced, which was associated with elevated HDAC1, HDAC4, and SIRT1 in colon adenocarcinomas. Results from this study revealed a novel anticancer mechanism of RARß via miR-22 induction to epigenetically regulate itself and NUR77, providing a promising cancer treatment modality using miR-22 and its inducers.-Hu, Y., French, S. W., Chau, T., Liu, H.-X., Sheng, L., Wei, F., Stondell, J., Garcia, J. C., Du, Y., Bowlus, C. L., Wan, Y.-J. Y. RARß acts as both an upstream regulator and downstream effector of miR-22, which epigenetically regulates NUR77 to induce apoptosis of colon cancer cells.

Microbial Intervention as a Novel Target in Treatment of Non-Alcoholic Fatty Liver Disease Progression.

BACKGROUND/AIMS: Emerging evidence suggests a close link between gut microbiota and non-alcoholic fatty liver disease (NAFLD). In this study, we aimed to investigate the association between gut microbiota and the DNA methylation of adiponectin (an adipocyte-specific adipocytokine) in rats, following diet-induced NAFLD. METHODS: 50 male SD rats were randomly divided into five groups with or without a high fat diet (HFD), antibiotics, and probiotics, in order to establish an imbalanced gut microbiota and probiotic treatment model in NAFLD rats. After 13 weeks of treatment, blood, liver, and cecal tissue samples were collected. Serum lipids, liver function indexes by biochemical analyzers, and changes in liver pathology with hematoxylin-eosin (HE) and masson staining were detected. Furthermore, the serum adiponectin by enzyme-linked immunosorbent assay (ELISA) and liver adiponectin methylation levels in the promoter regions by pyrophosphate sequencing were determined. High throughput Illumina sequencing targeted microbial 16S genes, bioinformatics and statistical analysis identified cecal-associated gut microbiota. RESULTS: HFD with antibiotic exposure showed the most severe steatohepatitis and a severe gut microbiota alteration. Reduced bacterial diversity was also seen and the abundances of Firmicutes, Lactobacillus, Cyanobacteria, Acidobacteria, Chlamydiae, Chlamydiales, Rubrobacteria, Verrucomicrobia, Blautia, Shewanella, Bacteroides, Bacteroides acidifaciens, and Bacteroides uniformis, were shown to be partly reversed by probiotic treatment. Decreased serum adiponectin levels and increased DNA methylation levels of adiponectin promoter regions were also markedly associated with the NAFLD progression during gut microbiota alteration. CONCLUSION: Our results suggested that both gut microbiota alteration and adiponectin variability may be drivers of NAFLD progression and that targeting the gut microbiota, such as via administration of a probiotic, may delay NAFLD progression via adiponectin.

Linc00483 as ceRNA regulates proliferation and apoptosis through activating MAPKs in gastric cancer.

Long non-coding RNAs (lncRNAs) are important regulators of many cellular processes, and their aberrant expression and/or function is associated with many different diseases, including cancer. However, the identification of functional lncRNAs in gastric cancer is still a challenge. In this study, we describe a novel functional lncRNA, linc00483, that is upregulated and associated with tumorigenesis, tumour size, metastasis and poor prognosis in gastric cancer. In our study, linc00483 promoted gastric cancer cell proliferation, invasiveness and metastasis in vitro and in vivo. Mechanistically, upregulated expression of linc00483 in gastric cancer acts as a sponge to absorb endogenous tumour suppressor miR-30a-3p. Furthermore, it restores SPAG9 expression, which is negatively regulated by miR-30a-3p, and actives MAPK signaling pathway in gastric cancer cells. Thus, linc00483 is an oncogenic lncRNA in gastric cancer and targeting linc00483 or its pathway can potentially be useful in development of targeted therapies for patients with gastric cancer. Our results show that linc00483 is an important regulator in carcinogenesis and may be a useful biomarker to predict prognosis of gastric cancer patients. We believe our findings are novel and will be of interest to scientists working in many areas related to biomarkers in cancer.

Alterations in the gut microbiota of patients with acquired immune deficiency syndrome.

Acquired immune deficiency syndrome (AIDS), caused by infection with human immunodeficiency virus (HIV), is associated with gastrointestinal disease, systemic immune activation and changes in the gut microbiota. Here, we aim to investigate the gut microbiota patterns of HIV-infected individuals and HIV-uninfected individuals in populations from South China. We enrolled 33 patients with HIV (14 participants treated with highly active antiretroviral therapy [HAART] for more than 3 months; the remaining 19 individuals had not received treatment) and 35 healthy controls (HC) for a cross-sectional comparison of gut microbiota using stool samples. Gut microbial communities were profiled by sequencing the bacterial 16S rRNA genes. Dysbiosis was more common among patients with AIDS compared with healthy individuals. Dysbiosis was characterized by decreased α-diversity, low mean counts of Bacteroidetes, Faecalibacterium, Prevotella, Bacteroides vulgatus, Dialister and Roseburia inulnivorans, and high mean counts of Proteobacteria, Enterococcus, Streptococcus, Lactobacillus, Lachnociostridium, Ruminococcus gnavus and Streptococcus vestibularis. Increased abundance of Bacilli was observed in homosexual patients. Proteobacteria were higher among heterosexual patients with HIV infections. Tenericutes were higher among patients with history of intravenous drug abuse. Restoration of gut microbiota diversity and a significant increase in abundance of Faecalibacterium, Blautia and Bacteroides were found in patients receiving HAART compared to those who did not receive. HIV infection-associated dysbiosis is characterized by decreased levels of α-diversity and Bacteroidetes, increased levels of Proteobacteria and the alterations of gut microbiota correlate with the route of HIV transmission. The imbalanced faecal microbiota of HIV infection is partially restored after therapy.

Genotypic Variation in Yield, Yield Components, Root Morphology and Architecture, in Soybean in Relation to Water and Phosphorus Supply.

Water shortage and low phosphorus (P) availability limit yields in soybean. Roots play important roles in water-limited and P-deficient environment, but the underlying mechanisms are largely unknown. In this study we determined the responses of four soybean [Glycine max (L.) Merr.] genotypes [Huandsedadou (HD), Bailudou (BLD), Jindou 21 (J21), and Zhonghuang 30 (ZH)] to three P levels [applied 0 (P0), 60 (P60), and 120 (P120) mg P kg-1 dry soil to the upper 0.4 m of the soil profile] and two water treatment [well-watered (WW) and water-stressed (WS)] with special reference to root morphology and architecture, we compared yield and its components, root morphology and root architecture to find out which variety and/or what kind of root architecture had high grain yield under P and drought stress. The results showed that water stress and low P, respectively, significantly reduced grain yield by 60 and 40%, daily water use by 66 and 31%, P accumulation by 40 and 80%, and N accumulation by 39 and 65%. The cultivar ZH with the lowest daily water use had the highest grain yield at P60 and P120 under drought. Increased root length was positively associated with N and P accumulation in both the WW and WS treatments, but not with grain yield under water and P deficits. However, in the WS treatment, high adventitious and lateral root densities were associated with high N and P uptake per unit root length which in turn was significantly and positively associated with grain yield. Our results suggest that (1) genetic variation of grain yield, daily water use, P and N accumulation, and root morphology and architecture were observed among the soybean cultivars and ZH had the best yield performance under P and water limited conditions; (2) water has a major influence on nutrient uptake and grain yield, while additional P supply can modestly increase yields under drought in some soybean genotypes; (3) while conserved water use plays an important role in grain yield under drought, root traits also contribute to high nutrient uptake efficiency and benefit yield under drought.

Pattern of Water Use and Seed Yield under Terminal Drought in Chickpea Genotypes.

Drought, particularly terminal drought, reduces the yield of chickpea (Cicer arietinum L.). Terminal drought tolerance and water use patterns were evaluated under controlled conditions in 10 genotypes of desi chickpea. Withholding water from early podding reduced vegetative growth, reproductive growth, seed yield, and water use efficiency for seed yield in all genotypes. The genotype Neelam, which produced the highest seed yield when water was withheld, used the least water when well-watered; however, its aboveground biomass at maturity did not differ significantly from six of the nine other genotypes. Indeed, the water-stressed Neelam had the lowest daily transpiration rate during the early stages of water stress and the highest during the later stages, thereby maintaining the highest soil water content in the first 16 days after water was withheld, which enabled higher pod production, lower pod abortion, and better seed filling. Genotypes differed in the threshold value of the fraction of transpirable soil water when flowering and seed set ceased in the water-stress treatment. We conclude that a conservative water use strategy benefits seed yield of chickpea exposed to water shortage during early podding.

Evolutionary agroecology: individual fitness and population yield in wheat (Triticum aestivum).

Although the importance of group selection in nature is highly controversial, several researchers have argued that plant breeding for agriculture should be based on group selection, because the goal in agriculture is to optimize population production, not individual fitness. A core hypothesis behind this claim is that crop genotypes with the highest individual fitness in a mixture of genotypes will not produce the highest population yield, because fitness is often increased by "selfish" behaviors, which reduce population performance. We tested this hypothesis by growing 35 cultivars of spring wheat (Triticum aestivum L.) in mixtures and monocultures, and analyzing the relationship between population yield in monoculture and individual yield in mixture. The relationship was unimodal, as predicted. The highest-yielding populations were from cultivars that had intermediate fitness, and these produced, on average, 35% higher yields than cultivars with the highest fitness. It is unlikely that plant breeding or genetic engineering can improve traits that natural selection has been optimizing for millions of years, but there is unutilized potential in traits that increase crop yield by decreasing individual fitness.