Morphological and chemical components of resistance to pod borer, Helicoverpa armigera in wild relatives of pigeonpea

Host plant resistance is an important component for minimizing the losses due to the pod borer, Helicoverpa armigera, which is the most devastating pest of pigeonpea. An understanding of different morphological and biochemical components of resistance is essential for developing strategies to breed for resistance to insect pests. Therefore, we studied the morphological and biochemical components associated with expression of resistance to H. armigera in wild relatives of pigeonpea to identify accessions with a diverse combination of characteristics associated with resistance to this pest. Among the wild relatives, oviposition non-preference was an important component of resistance in Cajanus scarabaeoides, while heavy egg-laying was recorded on C. cajanifolius (ICPW 28) and Rhynchosia bracteata (ICPW 214). Accessions belonging to R. aurea, C. scarabaeoides, C. sericeus, C. acutifolius, and Flemingia bracteata showed high levels of resistance to H. armigera, while C. cajanifolius was as susceptible as the susceptible check, ICPL 87. Glandular trichomes (type A) on the calyxes and pods were associated with susceptibility to H. armigera, while the non-glandular trichomes (trichome type C and D) were associated with resistance to this insect. Expression of resistance to H. armigera was also associated with low amounts of sugars and high amounts of tannins and polyphenols. Accessions of wild relatives of pigeonpea with non-glandular trichomes (type C and D) or low densities of glandular trichomes (type A), and high amounts of polyphenols and tannins may be used in wide hybridization to develop pigeonpea cultivars with resistance to H. armigera

Pod surface exudates of wild relatives of pigeonpea influence the feeding preference of the pod borer, Helicoverpa armigera

Wild relatives of crops are an important source of resistance genes against insect pests. However, it is important to identify the accessions of wild relatives of crops with different mechanisms of resistance to broaden the basis and increase the levels of resistance to insect pests. Therefore, we studied the feeding behavior of pod borer, Helicoverpa armigera, which is the most damaging pest of pigeonpea, in relation to biochemical characteristics of the pod surface exudates in a diverse array of germplasm accessions belonging to 12 species of pigeonpea wild relatives. Feeding by H. armigera larvae was significantly lower on the unwashed or water-, methanol-, or hexane-washed pods of Canajus sericeus, C. scarabaeoides, Flemingia bracteata, F. stricta, and Rhynchosia aurea than those of C. acutifolius, C. albicans, C. cajanifolius, C. lineatus, D. ferruginea, P. scariosa, R. bracteata, and the cultivated pigeonpea, C. cajan genotypes, ICPL 87, and ICPL 332, although there were a few exceptions. The methanol-washed pods of wild relatives were less preferred for feeding by the H. armigera larvae than the unwashed pods, but the hexane-washed pods were preferred more than the unwashed pods. The results suggested that methanol extracted the phagostimulants from the pod surface, while hexane removed the antifeedants. The high-performance liquid chromatography (HPLC) finger printing of methanol and hexane pod surface extracts showed qualitative and quantitative differences in compounds present on the pod surface of different wild relatives of pigeonpea. Some of the peaks in HPLC profiles were associated with feeding preference of the third-instar larvae of H. armigera. There was considerable diversity in wild relatives of pigeonpea as revealed by principal component analysis based on HPLC fingerprints of pod surface extracts in methanol and hexane, and H. armigera feeding on the pods. Wild pigeonpea accessions with low amounts of phagostimulants and high amounts of antifeedants may be used for introgression of resistance genes into the cultivated pigeonpea to develop varieties with broad-based resistance to H. armigera. There is considerable diversity among the wild relatives of pigeonpea, and the accessions with resistance to pod borer. These can be used to broaden the basis and increase the levels of resistance to H. armigera

Antixenosis and antibiosis components of resistance to pod borer Helicoverpa armigera in wild relatives of pigeonpea.

The legume pod borer (Helicoverpa armigera (Hubner)) is one of the most important pests of pigeonpea. The levels of resistance to H. armigera in the cultivated germplasm are quite low, and therefore there is a need to introgress resistance genes from wild relatives into the cultigen. We evaluated a diverse array of wild relatives of pigeonpea for oviposition non-preference and antibiosis components of resistance to H. armigera. The accessions ICPW 1 (Cajanus acutifolius), ICPW 13 and 14 (C. albicans), ICPW 159 and 160 (C. sericeus), ICPW 68 (C. platycarpus), ICPW 83, 90, 94, 125, 137, 141 and 280 (C. scarabaeoides), ICPW 207 (Paracalyx scariosa) and ICPW 210 (Rhynchosia aurea) showed high levels of antixenosis for oviposition under no-choice, dual-choice and multi-choice conditions. High levels of antibiosis were observed when the larvae were reared on leaves and/or pods of C. acutifolius (ICPW 1), C. cajanifolius (ICPW 29), C. sericeus (ICPW 160), P. scariosa (ICPW 207), C. scarabaeoides and C. albicans. Lyophilized leaf or pod powder incorporated into the artificial diet can be used to assess antibiosis to H. armigera, and high levels of antibiosis to H. armigera were observed in diets with leaf and/or pod powder of some of the accessions of C. acutifolius, C. lineatus, C. sericeus, C. scarabaeoides, C. platycarpus, P. scariosa and R. aurea. Post-embryonic development period was prolonged in insects reared on leaves and pods of wild relatives of pigeonpea. The accessions showing high levels of antixenosis and antibiosis can be used to increase the levels and diversify the bases of resistance to H. armigera in pigeonpea

Ets homologous factor (EHF) has critical roles in epithelial dysfunction in airway disease

The airway epithelium forms a barrier between the internal and external environments. Epithelial dysfunction is critical in the pathology of many respiratory diseases, including cystic fibrosis. Ets homologous factor (EHF) is a key member of the transcription factor network that regulates gene expression in the airway epithelium in response to endogenous and exogenous stimuli. EHF , which has altered expression in inflammatory states, maps to the 5' end of an intergenic region on Chr11p13 that is implicated as a modifier of cystic fibrosis airway disease. Here we determine the functions of EHF in primary human bronchial epithelial (HBE) cells and relevant airway cell lines. Using EHF ChIP followed by deep sequencing (ChIP-seq) and RNA sequencing after EHF depletion, we show that EHF targets in HBE cells are enriched for genes involved in inflammation and wound repair. Furthermore, changes in gene expression impact cell phenotype because EHF depletion alters epithelial secretion of a neutrophil chemokine and slows wound closure in HBE cells. EHF activates expression of the SAM pointed domain-containing ETS transcription factor, which contributes to goblet cell hyperplasia. Our data reveal a critical role for EHF in regulating epithelial function in lung disease

FGFR1 and NTRK3 actionable alterations in “Wild-Type” gastrointestinal stromal tumors

BACKGROUND: About 10–15% of adult, and most pediatric, gastrointestinal stromal tumors (GIST) lack mutations in KIT, PDGFRA, SDHx, or RAS pathway components (KRAS, BRAF, NF1). The identification of additional mutated genes in this rare subset of tumors can have important clinical benefit to identify altered biological pathways and select targeted therapies. METHODS: We performed comprehensive genomic profiling (CGP) for coding regions in more than 300 cancer-related genes of 186 GISTs to assess for their somatic alterations. RESULTS: We identified 24 GIST lacking alterations in the canonical KIT/PDGFRA/RAS pathways, including 12 without SDHx alterations. These 24 patients were mostly adults (96%). The tumors had a 46% rate of nodal metastases. These 24 GIST were more commonly mutated at 7 genes: ARID1B, ATR, FGFR1, LTK, SUFU, PARK2 and ZNF217. Two tumors harbored FGFR1 gene fusions (FGFR1–HOOK3, FGFR1–TACC1) and one harbored an ETV6–NTRK3 fusion that responded to TRK inhibition. In an independent sample set, we identified 5 GIST cases lacking alterations in the KIT/PDGFRA/SDHx/RAS pathways, including two additional cases with FGFR1–TACC1 and ETV6–NTRK3 fusions. CONCLUSIONS: Using patient demographics, tumor characteristics, and CGP, we show that GIST lacking alterations in canonical genes occur in younger patients, frequently metastasize to lymph nodes, and most contain deleterious genomic alterations, including gene fusions involving FGFR1 and NTRK3. If confirmed in larger series, routine testing for these translocations may be indicated for this subset of GIST. Moreover, these findings can be used to guide personalized treatments for patients with GIST. Trial registration NCT 02576431. Registered October 12, 2015 ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/s12967-016-1075-6) contains supplementary material, which is available to authorized users