01707nas a2200253   4500008004100000022001400041245005900055210005900114260007400173300001200247490000700259520089800266653002301164653001801187653002001205653002201225653001901247100002101266700001601287700002401303700001801327700001801345856009001363       2009                        eng d  a1380-374300aMolecular mapping of wilt resistance genes in chickpea0 aMolecular mapping of wilt resistance genes in chickpea  aVAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDSbSPRINGERcSEP  a177-1830 v243 a<p>Fusarium wilt is a widespread and serious chickpea disease caused by the soil-borne fungus Fusarium oxysporum f.sp. ciceri (Foc). We evaluated an F(9) recombinant inbred line population of chickpea for resistance to three Foc races (1, 2 and 3) in pot culture experiments and identified flanking and tightly linked DNA markers for the resistance genes. The simple sequence repeat markers H3A12 and TA110 flanked the Foc1 locus at 3.9 and 2.1 cM, respectively, while Foc2 was mapped 0.2 cM from TA96 and 2.7 cM from H3A12. The H1B06y and TA194 markers flanked the Foc3 locus at 0.2 and 0.7 cM, respectively. These markers were also validated using 16 diverse chickpea genotypes. Identification of tightly linked flanking markers for wilt resistance genes will be useful for their exploitation in breeding programs and to understand the mechanism of resistance and evolution of the genes.</p>10afusarium oxysporum10aFusarium wilt10aGenetic mapping10aMarker validation10aPathogen races1 aGowda, S., J. M.1 aRadhika, P.1 aKadoo, Narendra, Y.1 aMhase, L., B.1 aGupta, V., S.  uhttps://library.ncl.res.in/content/molecular-mapping-wilt-resistance-genes-chickpea-002495nas a2200277   4500008004100000022001400041245012300055210006900178260010600247300001200353490000800365520149500373653001301868653001801881653001001899653001701909653001201926653001601938100002001954700002601974700002602000700002402026700002002050700002102070856012602091       2015                        eng d  a0031-942200aMetabolic profiling of chickpea-Fusarium interaction identifies differential modulation of disease resistance pathways0 aMetabolic profiling of chickpeaFusarium interaction identifies d  aTHE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLANDbPERGAMON-ELSEVIER SCIENCE LTDcAUG  a120-1290 v1163 a<p>Chickpea is the third most widely grown legume in the world and mainly used as a vegetarian source of human dietary protein. Fusarium wilt, caused by Fusarium oxysporum f. sp. ciceri (Foc), is one of the major threats to global chickpea production. Host resistance is the best way to protect crops from diseases; however, in spite of using various approaches, the mechanism of Foc resistance in chickpea remains largely obscure. In the present study, non-targeted metabolic profiling at several time points of resistant and susceptible chickpea cultivars using high-resolution liquid chromatography-mass spectrometry was applied to better understand the mechanistic basis of wilt resistance or susceptibility. Multivariate analysis of the data (OPLS-DA) revealed discriminating metabolites in chickpea root tissue after Foc inoculation such as flavonoids, isoflavonoids, alkaloids, amino acids and sugars. Foc inoculated resistant plants had more flavonoids and isoflavonoids along with their malonyl conjugates. Many antifungal metabolites that were induced after Foc infection viz, aurantion-obstine beta-glucosides and querecitin were elevated in resistant cultivar. Overall, diverse genetic and biochemical mechanisms were operational in the resistant cultivar for Foc defense as compared to the susceptible plant. The resistant chickpea plants employed the above-mentioned metabolic pathways as potential defense strategy against Foc. (C) 2015 Elsevier Ltd. All rights reserved.</p>10aChickpea10aFusarium wilt10aLC-MS10aMetabolomics10aOPLS-DA10aPhytoalexin1 aKumar, Yashwant1 aDholakia, Bhushan, B.1 aPanigrahi, Priyabrata1 aKadoo, Narendra, Y.1 aGiri, Ashok, P.1 aGupta, Vidya, S.  uhttps://library.ncl.res.in/content/metabolic-profiling-chickpea-fusarium-interaction-identifies-differential-modulation-002869nas a2200253   4500008004100000022001400041245012500055210006900180260009000249300001200339490000700351520190100358653001802259653002402277653002102301653003402322653001902356653001102375100001802386700002102404700003702425700002102462856013202483       2015                        eng d  a0885-576500aRole of methyl jasmonate in the expression of mycorrhizal induced resistance against Fusarium oxysporum in tomato plants0 aRole of methyl jasmonate in the expression of mycorrhizal induce  a24-28 OVAL RD, LONDON NW1 7DX, ENGLANDbACADEMIC PRESS LTD- ELSEVIER SCIENCE LTDcOCT  a139-1450 v923 a<p>Arbuscular mycorrhiza (AM) colonization led to a decrease in the severity of fusarium wilt disease caused by Fusarium oxysporum f. sp. lycopersici in tomato plants. The involvement of two plant defense hormones, namely methyl jasmonate (MeJA) and salicylic acid (SA), in the expression of mycorrhiza induced resistance (MIR) against this vascular pathogen was studied in the AM colonized and non-colonized (controls) plants. Activity of lipoxygenase (LOX), which plays a role in jasmonic acid (JA) biosynthesis, as well as levels of methyl jasmonate (MeJA) increased in AM colonized plants as compared to controls, but did not show any further changes in response to F. oxysporum inoculation. On the other hand, activity of phenylalanine ammonia lyase (PAL), which is an enzyme from salicylic acid (SA) biosynthetic pathway, as well as SA levels, increased in both controls and AM colonized plants in response to application of F. oxysporum spores. Hence the JA and not the SA signalling pathway appeared to play a role in the expression of MIR against this vascular pathogen. The resistance observed in AM colonized plants was completely compromised when plants were treated with the JA biosynthesis inhibitor salicylhydroxamic acid (SHAM). This confirmed that the AM-induced increase in JA levels was involved in the expression of resistance toward F. oxysporum. The SA response gene pathogenesis-related 1 (PR1) showed an increased expression in response to F. oxysporum infection in SHAM treated AM colonized plants as compared to plants that were not treated with this JA inhibitor. This suggested the possibility that JA inhibited SA responses, at least in the roots. AM colonization therefore appeared to prime plants for improved tolerance against the vascular pathogen F. oxysporum, which was mediated through the JA signalling pathway. (C) 2015 Elsevier Ltd. All rights reserved.</p>10aFusarium wilt10aGlomus fasciculatum10aMethyl jasmonate10aMycorrhiza induced resistance10aSalicylic acid10aTomato1 aNair, Aswathy1 aKolet, Swati, P.1 aThulasiram, Hirekodathakallu, V.1 aBhargava, Sujata  uhttps://library.ncl.res.in/content/role-methyl-jasmonate-expression-mycorrhizal-induced-resistance-against-fusarium-oxysporum-0