Modelling the impact of cabbage stem flea beetle larval feeding on oilseed rape lodging risk.

BACKGROUND: Cabbage stem flea beetle (CSFB, Psylliodes chrysocephala L.) is a major pest of oilseed rape (OSR, Brassica napus L.) in the UK and low availability of effective chemical control has increased the need for integrated pest management approaches. The risk of OSR to lodging is strongly related to stem strength, however, the impact of CSFB larval tunnelling on stem strength and subsequent risk to stem lodging is unknown. The study investigated this by applying the Generalised Crop Lodging Model to conventionally grown OSR crops scored for varying levels of CSFB larval tunnelling. Lodging risk mitigation strategies including plant growth regulators (PGR) and varying nitrogen regimes were tested under high CSFB larval pressure. RESULTS: Stems of OSR plants were categorised by the proportion of visual damage (< 5%; 5-25%; 26-50%; 51-75%; 75-100%). Stems of 26-50% damage had significantly lower breaking strengths and diameters compared to plants that scored < 5%, with the associated reduction in stem failure windspeed equivalent to an order of magnitude increase in the risk of a lodging event occurring in the UK. PGR use reduced plant height and subsequently lodging risk variably across the sites. CONCLUSION: Estimating the proportion of stem tunnelling alongside larval pressure may be a useful tool in considering the contribution of CSFB pressure to lodging risk. The research demonstrates that the use of canopy management principles to optimise canopy size through nitrogen management and PGR use may help offset increased lodging risk caused by CSFB tunnelling. © 2024 Society of Chemical Industry.

Expression of AS3MT alters transcriptional profiles in human urothelial cells exposed to arsenite.

Inorganic arsenic (iAs) is an environmental toxicant and human carcinogen. The enzymatic methylation of iAs that is catalyzed by arsenic (+3 oxidation state)-methyltransferase (AS3MT) generates reactive methylated intermediates that contribute to the toxic and carcinogenic effects of iAs. We have shown that clonal human urothelial cells (UROtsa/F35) that express rat AS3MT and methylate iAs are more susceptible to acute toxicity of arsenite (iAs(III)) than parental UROtsa cells that do not express AS3MT and do not methylate iAs. The current work examines transcriptional changes associated with AS3MT expression and identifies specific categories of genes expressed in UROtsa and UROtsa/F35 cells in response to a 24-h exposure to 1 or 50 microM iAs(III). Here, the expression of 21,073 genes was assessed using Agilent Human 1A(V2) arrays. Venn analysis showed marked concentration-dependent differences between gene expression patterns in UROtsa and UROTsa/F35 cells exposed to iAs(III). Among 134 genes altered by exposure to subtoxic 1 microM iAs(III), only 14 were shared by both cell lines. Exposure to cytotoxic 50 microM iAs(III) uniquely altered 1389 genes in UROtsa/F35 and 649 genes in UROtsa cells; 5033 altered genes were associated with the chemical alone. In UROtsa, but not UROtsa/F35 cells exposure to 1 microM iAs(III) altered expression of genes associated with cell adhesion. In contrast, expression of genes involved in cell cycle regulation was significantly altered in UROtsa/F35 cells at this exposure level. At 50 microM iAs(III), pathways regulating cell cycle, cell death, transcription, and metabolism were affected in both cell lines. However, only Urotsa/F35 cells showed numerous G-protein and kinase pathway alterations as well as alterations in pathways involved in cell growth and differentiation. These data link the AS3MT-catalyzed methylation of iAs to specific genomic responses in human cells exposed to iAs(III). Further analysis of these responses will help to characterize the role of AS3MT-catalyzed methylation in modulation of iAs(III) toxicity.

Iron superoxide dismutase protects against chilling damage in the cyanobacterium synechococcus species PCC7942

A strain of Synechococcus sp. PCC7942 lacking functional Fe superoxide dismutase (SOD), designated sodB-, was characterized by its growth rate, photosynthetic pigments, inhibition of photosynthetic electron transport activity, and total SOD activity at 0 degrees C, 10 degrees C, 17 degrees C, and 27 degrees C in moderate light. At 27 degrees C, the sodB- and wild-type strains had similar growth rates, chlorophyll and carotenoid contents, and cyclic photosynthetic electron transport activity. The sodB- strain was more sensitive to chilling stress at 17 degrees C than the wild type, indicating a role for FeSOD in protection against photooxidative damage during moderate chilling in light. However, both the wild-type and sodB- strains exhibited similar chilling damage at 0 degrees C and 10 degrees C, indicating that the FeSOD does not provide protection against severe chilling stress in light. Total SOD activity was lower in the sodB- strain than in the wild type at 17 degrees C and 27 degrees C. Total SOD activity decreased with decreasing temperature in both strains but more so in the wild type. Total SOD activity was equal in the two strains when assayed at 0 degrees C.

A cyanobacterium lacking iron superoxide dismutase is sensitized to oxidative stress induced with methyl viologen but Is not sensitized to oxidative stress induced with norflurazon

A strain of Synechococcus sp. strain PCC 7942 with no functional Fe superoxide dismutase (SOD), designated sodB-, was characterized by its growth rate, photosynthetic pigments, and cyclic photosynthetic electron transport activity when treated with methyl viologen or norflurazon (NF). In their unstressed conditions, both the sodB- and wild-type strains had similar chlorophyll and carotenoid contents and catalase activity, but the wild type had a faster growth rate and higher cyclic electron transport activity. The sodB- was very sensitive to methyl viologen, indicating a specific role for the FeSOD in protection against superoxide generated in the cytosol. In contrast, the sodB- mutant was less sensitive than the wild type to oxidative stress imposed with NF. This suggests that the FeSOD does not protect the cell from excited singlet-state oxygen generated within the thylakoid membrane. Another up-regulated antioxidant, possibly the MnSOD, may confer protection against NF in the sodB- strain. These results support the hypothesis that different SODs have specific protective functions within the cell.