BackgroundSunflower Verticillium wilt (SVW) is a vascular disease caused by root infection with Verticillium dahliae (V. dahlia). It is a serious threat to the yield and quality of sunflower. However, chemical and agronomic measures for controlling this disease are not effective. The selection of more resistant genotypes is a desirable strategy to reduce contamination. A deeper knowledge of the molecular mechanisms and genetic basis underlying sunflower Verticillium wilt is necessary to accelerate breeding progress.ResultsAn RNA-Seq approach was used to perform global transcriptome profiling on the roots of resistant (S18) and susceptible (P77) sunflower genotypes infected with V. dahlia. Different pairwise transcriptome comparisons were examined over a time course (6, 12 and 24 h, and 2, 3, 5 and 10 d post inoculation). In RD, SD and D datasets, 1231 genes were associated with SVW resistance in a genotype-common transcriptional pattern. Moreover, 759 and 511 genes were directly related to SVW resistance in the resistant and susceptible genotypes, respectively, in a genotype-specific transcriptional pattern. Most of the genes were demonstrated to participate in plant defense responses; these genes included peroxidase (POD), glutathione peroxidase, aquaporin PIP, chitinase, L-ascorbate oxidase, and LRR receptors. For the up-regulated genotype-specific differentially expressed genes (DEGs) in the resistant genotype, higher average fold-changes were observed in the resistant genotype compared to those in the susceptible genotype. An inverse effect was observed in the down-regulated genotype-specific DEGs in the resistant genotype. KEGG analyses showed that 98, 112 and 52 genes were classified into plant hormone signal transduction, plant-pathogen interaction and flavonoid biosynthesis categories, respectively. Many of these genes, such as CNGC, RBOH, FLS2, JAZ, MYC2 NPR1 and TGA, regulate crucial points in defense-related pathway and may contribute to V. dahliae resistance in sunflower.ConclusionsThe transcriptome profiling results provided a clearer understanding of the transcripts associated with the crosstalk between sunflower and V. dahliae. The results identified several differentially expressed unigenes involved in the hyper sensitive response (HR) and the salicylic acid (SA)/jasmonic acid (JA)-mediated signal transduction pathway for resistance against V. dahliae. These results are useful for screening resistant sunflower genotypes.Electronic supplementary materialThe online version of this article (doi:10.1186/s12864-016-3386-7) contains supplementary material, which is available to authorized users.

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Sequences with low auto-correlation property have been applied in code-division multiple access communication systems, radar and cryptography. Using the inverse Gray mapping, a quaternary sequence of even length N can be obtained from two binary sequences of the same length, which are called component sequences. In this paper, using interleaving method, we present several classes of component sequences from twin-prime sequences pairs or GMW sequences pairs given by Tang and Ding in 2010; two, three or four binary sequences defined by cyclotomic classes of order 4. Hence we can obtain new classes of quaternary sequences, which are different from known ones, since known component sequences are constructed from a pair of binary sequences with optimal auto-correlation or Sidel'nikov sequences.The cross-correlation function R s,t (τ ) between s and t is defined by

Binary sequences with optimal autocorrelation play important roles in radar, communication, and cryptography. Finding new binary sequences with optimal autocorrelation has been an interesting research topic in sequence design. Ding-Helleseth-Lam sequences are such a class of binary sequences of period p, where p is an odd prime with p ≡ 1(mod 4). The objective of this letter is to present a construction of binary sequences of period 4p via interleaving four suitable Ding-Helleseth-Lam sequences. This construction generates new binary sequences with optimal autocorrelation which can not be produced by earlier ones.

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Background:A germline deletion in BIM (B cell lymphoma-2-like 11) gene has been shown to impair the apoptotic response to epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs) in vitro but its impact on response to EGFR-TKIs in patients of nonsmall cell lung cancer (NSCLC) remains controversial.Methods:Eligible literature were searched and screened. Objective response rate (ORR) and disease control rate (DCR) were extracted and aggregated with odds ratio (OR). Hazard ratio (HR) and 95% confidence interval (CI) for progression-free survival (PFS) and overall survival (OS) were extracted and aggregated based on random-effect model.Results:Fourteen studies including 2694 NSCLC patients were eligible. Individuals harboring BIM deletion polymorphism had inferior ORR (OR = 0.49, 95% CI: 0.34–0.70, P < .001), inferior DCR (OR = 0.50, 95% CI: 0.30–0.84, P = .009). Patients with BIM deletion had shorter OS despite of the heterogeneity between countries (in subgroup of South Korea and Taiwan, HR = 1.34, 95% CI: 1.18–1.53, P < .001; in subgroup of other countries, HR = 2.43, 95% CI: 2.03–2.91, P < .001). The pooled analysis of PFS showed great heterogeneity (I2 = 79%). All the reported characteristics did not account for the heterogeneity. However, 2 subgroups could be obtained through sensitivity analysis. In one subgroup, patients with BIM deletion polymorphism had shorter PFS (HR = 2.03, 95% CI: 1.71–2.40, P < .001), while in the other subgroup, no significant difference was observed (HR = 0.92, 95% CI: 0.79–1.06, P = .25).Conclusion:NSCLC patients with BIM deletion polymorphism show poor ORR, DCR, and OS after EGFR-TKIs treatment. BIM deletion polymorphism indicates poor response to EGFR-TKIs, and it could be used as a predictor to identify those who would benefit from EGFR-TKIs in NSCLC patients.

We show that the contact process on a random d-regular graph initiated by a single infected vertex obeys the "cutoff phenomenon" in its supercritical phase. In particular, we prove that when the infection rate is larger than the critical value of the contact process on the infinite d-regular tree there are positive constants C, p depending on the infection rate such that for any ε > 0, when the number n of vertices is large then (a) at times t < (C − ε) log n the fraction of infected vertices is vanishingly small, but (b) at time (C + ε) log n the fraction of infected vertices is within ε of p, with probability p.