Cross talk between phytohormones, nitric oxide (NO), and auxin has been implicated in the control of plant growth and development. Two recent reports indicate that NO promoted auxin signaling but inhibited auxin transport probably through S-nitrosylation. However, genetic evidence for the effect of S-nitrosylation on auxin physiology has been lacking. In this study, we used a genetic approach to understand the broader role of S-nitrosylation in auxin physiology in Arabidopsis. We compared auxin signaling and transport in Col-0 and gsnor1-3, a loss-of-function GSNOR1 mutant defective in protein de-nitrosylation. Our results showed that auxin signaling was impaired in the gsnor1-3 mutant as revealed by significantly reduced DR5-GUS/DR5-GFP accumulation and compromised degradation of AXR3NT-GUS, a useful reporter in interrogating auxin-mediated degradation of Aux/IAA by auxin receptors. In addition, polar auxin transport was compromised in gsnor1-3, which was correlated with universally reduced levels of PIN or GFP-PIN proteins in the roots of the mutant in a manner independent of transcription and 26S proteasome degradation. Our results suggest that S-nitrosylation and GSNOR1-mediated de-nitrosylation contribute to auxin physiology, and impaired auxin signaling and compromised auxin transport are responsible for the auxin-related morphological phenotypes displayed by the gsnor1-3 mutant.

Quantitative trait loci (QTL) contributing to the frequency and severity of Ustilago maydis infection in the leaf, ear, stalk, and tassel of maize plants were mapped using an A188 x CMV3 and W23 x CMV3 recombinant inbred (RI) populations. QTLs mapped to genetic bins 2.04 and 9.04-9.05 of the maize genome contributed strongly (R (2) = 18-28%) to variation in the frequency and severity of U. maydis infection over the entire plant in both populations and within the majority of environments. QTLs mapped to bins 3.05, 3.08, and 8.00 in the A188 x CMV3 population and bin 4.05 in both populations significantly contributed to the frequency or severity of infection in only the tassel tissue. QTLs mapped to bin 1.07 in the A188 x CMV3 population and bin 7.00 in the W23 x CMV3 population contributed to U. maydis resistance in only the ear tissue. Interestingly, the CMV3 allele of the QTL mapped to bin 1.10 in the A188 x CMV3 population significantly contributed to U. maydis susceptibility in the ear and stalk but significantly increased resistance in the tassel tissue. Digenic epistatic interactions between the QTL mapped to bin 5.08 and four distinct QTLs significantly contributed to the frequency and severity of infection over the entire plant and within the tassel tissue of the A188 x CMV3 population. Several QTLs detected in this study mapped to regions of the maize genome containing previously mapped U. maydis resistance QTLs and genes involved in plant disease resistance.

Oat-maize addition (OMA) lines with one, or occasionally more, chromosomes of maize (Zea mays L., 2n = 2x = 20) added to an oat (Avena sativa L., 2n = 6x = 42) genomic background can be produced via embryo rescue from sexual crosses of oat x maize. Self-fertile disomic addition lines of different oat genotypes, mainly cultivar Starter, as recipient for maize chromosomes 1, 2, 3, 4, 5, 6, 7, 9, and the short arm of 10 and a monosomic addition line for chromosome 8, have been reported previously in which the sweet corn hybrid Seneca 60 served as the maize chromosome donor. Here we report the production and characterization of a series of new OMA lines with inbreds B73 and Mo17 as maize chromosome donors and with oat cultivars Starter and Sun II as maize chromosome recipients. Fertile disomic OMA lines were recovered for B73 chromosomes 1, 2, 4, 5, 6, 8, 9, and 10 and Mo17 chromosomes 2, 4, 5, 6, 8, and 10. These lines together with non-fertile (oat x maize) F(1) plants with chromosome 3 and chromosome 7 of Mo17 individually added to Starter oat provide DNA of additions to oat of all ten individual maize chromosomes between the two maize inbreds. The Mo17 chromosome 10 OMA line was the first fertile disomic OMA line obtained carrying a complete chromosome 10. The B73 OMA line for chromosome 1 and the B73 and Mo17 OMA lines for chromosome 8 represent disomic OMA lines with improved fertility and transmission of the addition chromosome compared to earlier Seneca 60 versions. Comparisons among the four oat-maize parental genotype combinations revealed varying parental effects and interactions on frequencies of embryo recovery, embryo germination, F(1) plantlets with maize chromosomes, the specific maize chromosomes retained and transmitted to F(2) progeny, and phenotypes of self-fertile disomic addition plants. As opposed to the previous use of a hybrid Seneca 60 maize stock as donor of the added maize chromosomes, the recovered B73 and Mo17 OMA lines provide predictable genotypes for use as tools in physical mapping of maize DNA sequences, including inter-genic sequences, by simple presence/absence assays. The recovered OMA lines represent unique materials for maize genome analysis, genetic, physiological, and morphological studies, and a possible means to transfer maize traits to oat. Descriptions of these materials can be found at http://agronomy.cfans.umn.edu/Maize_Genomics.html .

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