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Fusarium oxysporum is a root-infecting fungal pathogen that causes wilt disease on a broad range of plant species, including the model plant Arabidopsis thaliana. Currently, very little is known about the molecular or physiological processes that are activated in the host during infection and the roles these processes play in resistance and susceptibility to F. oxysporum. In this study, we analyzed global gene expression profiles of F. oxysporum-infected Arabidopsis plants. Genes involved in jasmonate biosynthesis as well as jasmonate-dependent defense were coordinately induced by F. oxysporum. Similarly, tryptophan pathway genes, including those involved in both indole-glucosinolate and auxin biosynthesis, were upregulated in both the leaves and the roots of inoculated plants. Analysis of plants expressing the DR5:GUS construct suggested that root auxin homeostasis was altered during F. oxysporum infection. However, Arabidopsis mutants with altered auxin and tryptophan-derived metabolites such as indole-glucosinolates and camalexin did not show an altered resistance to this pathogen. In contrast, several auxin-signaling mutants were more resistant to F. oxysporum. Chemical or genetic alteration of polar auxin transport also conferred increased pathogen resistance. Our results suggest that, similarly to many other pathogenic and nonpathogenic or beneficial soil organisms, F. oxysporum requires components of auxin signaling and transport to colonize the plant more effectively. Potential mechanisms of auxin signaling and transport-mediated F. oxysporum susceptibility are discussed.

Fifty sequence-tagged microsatellite site (STMS) markers and a resistant gene-analog (RGA) locus were integrated into a chickpea ( Cicer arietinum L., 2n = 2 x = 16 chromosomes) genetic map that was previously constructed using 142 F(6)-derived recombinant inbred lines (RILs) from a cross of C. arietinum x Cicer reticulatum Lad. The map covers 1,174.5 cM with an average distance of 7.0 cM between markers in nine linkage groups (LGs). Nine markers including the RGA showed distorted segregation ( P < 0.05). The majority of the newly integrated markers were mapped to marker-dense regions of the LGs. Six co-dominant STMS markers were integrated into two previously reported major quantitative trait loci (QTLs) conferring resistance to Ascochyta blight caused by Ascochyta rabiei (Pass.) Labr. Using common STMS markers as anchors, three maps developed from different mapping populations were joined, and genes for resistance to Ascochyta blight, Fusarium wilt (caused by Fusarium oxysporum Schlechtend.: Fr. f. sp. ciceris), and for agronomically important traits were located on the combined linkage map. The integration of co-dominant STMS markers improves the map of chickpea and makes it possible to consider additional fine mapping of the genome and also map-based cloning of important disease resistance genes.

Ascochyta blight, caused by Ascochyta rabiei (Pass.) Lab., is a devastating disease of chickpea (Cicer arietinum L.) worldwide. Resistant germplasm has been identified and the genetics of resistance has been the subject of numerous studies. The objectives of the present study were to determine the genetics of resistance to ascochyta blight of chickpea and to map and tag the chromosomal regions involved using molecular markers. We used a set of 142 F5:6 recombinant inbred lines (RILs) obtained from an interspecific cross of C. arietinum (FLIP84‐92C, resistant parent) × C. reticulatum Lad. (PI 599072, susceptible parent). The RILs were scored for disease reactions in the field over 2 yr and were genotyped for polymorphic molecular markers [isozyme, random amplified polymorphic DNA (RAPD), and inter simple sequence repeat (ISSR)] in the laboratory. The disease was scored quantitatively and data were used for QTL analysis. A linkage map was established that comprised nine linkage groups containing 116 markers covering a map distance of 981.6 centimorgans (cM) with an average distance of 8.4 cM between markers. Two quantitative trait loci (QTLs), QTL‐1 and QTL‐2, conferring resistance to ascochyta blight, were identified which accounted for 50.3 and 45.0% of the estimated phenotypic variation in 1997 and 1998, respectively, and were mapped to linkage groups 6 and 1, respectively. Two RAPD markers flanked QTL‐1 and were 10.9 cM apart while one ISSR marker and an isozyme marker flanked QTL‐2 and were 5.9 cM apart. These markers can be used for marker‐assisted selection for ascochyta blight resistance in chickpea breeding programs, and to develop durable resistant cultivars through gene pyramiding.

A consensus genetic map of chickpea (Cicer arietinum L.) was constructed by merging linkage maps from 10 different populations, using STMS (Sequence-tagged Microsatellite Sites) as bridging markers. These populations derived from five wide crosses (C. arietinum 9 Cicer reticulatum) and five narrow crosses (Desi 9 Kabuli types) were previously used for mapping genes for several agronomic traits such as ascochyta blight, fusarium wilt, rust resistance, seed weight, flowering time and days to flower. The integrated map obtained from wide crosses consists of 555 loci including, among other markers, 135 STMSs and 33 cross-genome markers distributed on eight linkage groups and covers 652.67 cM. The map obtained from narrow crosses comprises 99 STMSs, 3 SCARs, 1 ASAP, fusarium resistance gene, 5 morphological traits as well as RAPD and ISSR markers distributed on eight linkage groups covering 426.99 cM. Comparison between maps from wide and narrow crosses reflects a general coincidence, Electronic supplementary material The online version of this article (