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In insects, vitellogenin (Vg) is generally viewed as a female‐specific protein. Its primary function is to supply nutrition to developing embryos. Here, we reported Vg from the male adults of a natural predator, Chrysopa pallens. The male Vg was depleted by RNAi. Mating with Vg‐deficient male downregulated female Vg expression, suppressed ovarian development and decreased reproductive output. Whole‐organism transcriptome analysis after male Vg knockdown showed no differential expression of the known spermatogenesis‐related regulators and seminal fluid protein genes, but a sharp downregulation of an unknown gene, which encodes a testis‐enriched big protein (Vcsoo). Separate knockdown of male Vg and Vcsoo disturbed the assembly of spermatid cytoplasmic organelles in males and suppressed the expansion of ovary germarium in mated females. These results demonstrated that C. pallens male Vg signals through the downstream Vcsoo and regulates male and female reproduction. [ABSTRACT FROM AUTHOR]

Background and objective: Host immunity is crucial during periodontal inflammations. B cells are considered to have a function of immunoregulation, and TLRs are considered to be crucial in this process. The present study illustrates the potential roles and rules of CD25+ B cells during periodontitis, especially its effect on regulating host IL‐35 level and Th1, Th17, and Treg differentiation. Material and methods: The proportion of local and systemic CD25+ B cell subpopulations from periodontitis models were identified by flow cytometry. To illustrate further mechanism, B cells were cultured with a different type of TLR activators. Expression of IL‐10, IL‐35, and TGF‐β was detected by ELISA and real‐time PCR. We also set adoptive transfer models by using CD25+ B cells. Alveolar bone erosion, proportion of Th1, Th17, and Tregs, and levels of IFN‐γ, TNF‐α, IL‐1β, and IL‐17 were identified. Result: Periodontitis induces more CD25+ B cell subpopulations and promotes their IL‐10, IL‐35, and TGF‐βproduction. TLR activators enhanced Breg proliferation and function. LPS+CpG obviously induced more CD25+ B cell differentiation and production of IL‐10, IL‐35, and TGF‐β. Adoptive transfer of CD25+ B cells reduces alveolar bone destruction and local Tregs, proportion, especially the local level of IFN‐γ and IL‐17. In addition, adoptive transfer of CD25+ B cells remedies the pathological change in the proportion of IL‐1β and Th1/Th17 in local lesions. We did not find any significant difference in peripheral blood, regardless of group and detected items. Conclusion: Results of the present study clarify that CD25+ B cells enlarged and produced more IL‐10, IL‐35 and TGF‐β during periodontitis, activation of TLR4 and TLR9 played crucial roles in this process. Also, CD25+ B cells alleviated periodontal inflammation and alveolar bone resorption. Our findings further expanded the potential of B cells during periodontitis. [ABSTRACT FROM AUTHOR]

To explore the mechanisms of 5‐aminolevulinic acid (ALA)‐improved plant salt tolerance, strawberries (Fragaria × ananassa Duch. cv. 'Benihoppe') were treated with 10 mg l−1 ALA under 100 mmol l−1 NaCl stress. We found that the amount of Na+ increased in the roots but decreased in the leaves. Laser scanning confocal microscopy (LSCM) observations showed that ALA‐induced roots had more Na+ accumulation than NaCl alone. Measurement of the xylem sap revealed that ALA repressed Na+ concentrations to a large extent. The electron microprobe X‐ray assay also confirmed ALA‐induced Na+ retention in roots. qRT‐PCR showed that ALA upregulated the gene expressions of SOS1 (encoding a plasma membrane Na+/H+ antiporter), NHX1 (encoding a vacuolar Na+/H+ antiporter) and HKT1 (encoding a protein of high‐affinity K+ uptake), which are associated with Na+ exclusion in the roots, Na+ sequestration in vacuoles and Na+ unloading from the xylem vessels to the parenchyma cells, respectively. Furthermore, we found that ALA treatment reduced the H2O2 content in the leaves but increased it in the roots. The exogenous H2O2 promoted plant growth, increased root Na+ retention and stimulated the gene expressions of NHX1, SOS1 and HKT1. Diphenyleneiodonium (DPI), an inhibitor of H2O2 generation, suppressed the effects of ALA or H2O2 on Na+ retention, gene expressions and salt tolerance. Therefore, we propose that ALA induces H2O2 accumulation in roots, which mediates Na+ transporter gene expression and more Na+ retention in roots, thereby improving plant salt tolerance. [ABSTRACT FROM AUTHOR]

Following superficial injury, neighbouring gastric epithelial cells close the wound by rapid cell migration, a process called epithelial restitution. Na+/H+ exchange (NHE) inhibitors interfere with restitution, but the role of the different NHE isoforms expressed in gastric pit cells has remained elusive. The role of the basolaterally expressed NHE1 (Slc9a1) and the presumably apically expressed NHE2 (Slc9a2) in epithelial restitution was investigated in the nontransformed rat gastric surface cell line RGM1. Migration velocity was assessed by loading the cells with the fluorescent dye DiR and following closure of an experimental wound over time. Since RGM1 cells expressed very low NHE2 mRNA and have low transport activity, NHE2 was introduced by lentiviral gene transfer. In medium with pH 7.4, RGM1 cells displayed slow wound healing even in the absence of growth factors and independently of NHE activity. Growth factors accelerated wound healing in a partly NHE1-dependent fashion. Preincubation with acidic pH 7.1 stimulated restitution in a NHE1-dependent fashion. When pH 7.1 was maintained during the restitution period, migratory speed was reduced to ∼10% of the speed at pH 7,4, and the residual restitution was further inhibited by NHE1 inhibition. Lentiviral NHE2 expression increased the steady-state pHi and reduced the restitution velocity after low pH preincubation, which was reversible by pharmacological NHE2 inhibition. The results demonstrate that in RGM1 cells, migratory velocity is increased by NHE1 activation, while NHE2 activity inhibit this process. A differential activation of NHE1 and NHE2 may therefore, play a role in the initiation and completion of the epithelial restitution process. [ABSTRACT FROM AUTHOR]

Previous studies have indicated thatArabidopsis thalianaexperienced a genome-wide duplication event shortly before its divergence fromBrassicafollowed by extensive chromosomal rearrangements and deletions. While a large number of the duplicated genes have significantly diverged or lost their sister genes, we found 4222 pairs that are still highly conserved, and as a result had similar functional assignments during the annotation of the genome sequence. Using whole-genome DNA microarrays, we identified 906 duplicated gene pairs in which at least one member exhibited a significant response to oxidative stress. Among these, only 117 pairs were up- or down-regulated in both pairs and many of these exhibited dissimilar patterns of expression. Examination of the expression patterns ofPAL1andPAL2,ACD1andACD2, genes coding for two Hsp20s, various P450s, and electron transfer flavoproteins suggests Arabidopsis evolved a number of distinct oxidative stress response mechanisms using similar gene sets following the duplication of its genome. [ABSTRACT FROM AUTHOR]

Myopodin was identified as a tumor suppressor gene that is frequently deleted in aggressive prostate cancer. Expression of myopodin protein suppresses both tumor growth and metastasis in vitro and in vivo. In the present study employing a yeast two-hybrid system, we found that zyxin, a molecule known to regulate cell motility and migration, binds with myopodin with high affinity. The binding between zyxin and myopodin appears to be direct. Screening of a series of myopodin deletion mutants and peptide competition analyses revealed that myopodin is bound by zyxin at a site located within the sequence of the 19 amino acids at the myopodin C-terminus. Importantly, this is the same region where the tumor suppressor activity of myopodin is located. The motility and invasion suppression activity of myopodin were significantly weakened in myopodin mutants lacking this sequence. Thus our studies suggest that zyxin may be a critical functional regulator of myopodin. [ABSTRACT FROM AUTHOR]