SummaryGynoecia of the Arabidopsis mutant sty1-1 display abnormal style morphology and altered vascular patterning. These phenotypes, which are enhanced in the sty1-1 sty2-1 double mutant, suggest that auxin homeostasis or signalling might be affected by mutations in STY1 and STY2, both members of the SHI gene family. Chemical inhibition of polar auxin transport (PAT) severely affects the apical-basal patterning of the gynoecium, as do mutations in the auxin transport/signalling genes PIN1, PID and ETT. Here we show that the apical-basal patterning of sty1-1 and sty1-1 sty2-1 gynoecia is hypersensitive to reductions in PAT, and that sty1-1 enhances the PAT inhibition-like phenotypes of pin1-5, pid-8 and ett-1 gynoecia. Furthermore, we show that STY1 activates transcription of the flavin monooxygenase-encoding gene THREAD/YUCCA4, involved in auxin biosynthesis, and that changes in expression of STY1 and related genes lead to altered auxin homeostasis. Our results suggest that STY1 and related genes promote normal development of the style and affect apical-basal patterning of the gynoecium through regulation of auxin homeostasis.

Abscisic acid (ABA) is a defense hormone with influence on callose-dependent and -independent resistance against Leptosphaeria maculans acting in the RLMcol pathway. ABA-deficient and -insensitive mutants in Ler-0 background (abal-3 and abil-1) displayed susceptibility to L. maculans, along with a significantly decreased level of callose depositions, whereas abi2-1 and abi3-1 remained resistant, together with the abi5-1 mutant of Ws-0 background. Suppressor mutants of abil-1 confirmed that the L. maculans-susceptible response was due to the dominant negative nature of the abil-1 mutant. Highly induced camalexin levels made ABA mutants in Col-0 background (aba2-1, aba3-1, and abi4-1) appear resistant, but displayed enhanced susceptibility as double mutants with pad3-1, impaired in camalexin biosynthesis. beta-Aminobutyric acid (BABA) pretreatment of Ler-0 contributed to an elevated level of endogenous ABA after L. maculans inoculation. Comparisons between (RLM1co1)pad3 and rlmlLerpad3 showed that ABA and BABA enhancement of callose deposition requires induction from RLM1col. ABII, but not ABI2, was found to be involved in a feedback mechanism that modulates RLM1co, expression. Genetic analysis showed further that this feedback occurs upstream of ABI4 and that components downstream of ABI4 modulate ABIJ activity. ABA and BABA treatments of the L. maculans-susceptible callose synthase mutant pmr4 showed that ABA also induces a callose-independent resistance. Similar treatments enhanced callose depositions and induced resistance to L. maculans in oilseed rape, and BABA-induced resistance was found to be independent of salicylic acid.

BackgroundExtended-spectrum cephalosporin-resistant Enterobacteriaceae (ESCRE) are an increasing healthcare problem in both human and veterinary medicine. The spread of ESCRE is complex with multiple reservoirs and different transmission routes. The aim of this study was to investigate if ESCRE carriage in dogs is more prevalent in households with a known human carrier, compared to households where humans are known to be negative for ESCRE. Identical ESCRE strains in humans and dogs of the same household would suggest a possible spread between humans and dogs.MethodsTwenty-two dog owners with a positive rectal culture for ESCRE each collected a rectal sample from their dog. In addition, a control group of 29 healthy dog owners with a documented negative rectal culture for ESCRE each sampled their household dog. Samples were cultivated for ESCRE using selective methods. In households where both humans and dogs carried ESCRE, isolates were further analysed for antimicrobial susceptibility by disc diffusion or microdilution and for genotype and genetic relatedness using molecular methods.ResultsIn 2 of 22 households studied, identical ESCRE strains with respect to bacterial species, antibiogram, genotype, and MLVA type were found in humans and dogs. The ESCRE found in the two households were ESBL-producing E. coli with the resistance gene blaCTX-M-27 and AmpC-producing E. coli with blaCMY-2, blaTEM-1. ESCRE were not found in dogs in the control group.ConclusionsIn households where humans are carrying ESCRE, identical strains were to a limited extent found also in household dogs, indicating a transfer between humans and dogs. In contrast, ESCRE were not found in dogs in households without human carriers.

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