Fusarium head blight (FHB) can contaminate cereal grains with mycotoxins. Winter wheat can also become infected with FHB and is more resistant than durum wheat to head infection but less than other small-grain cereals. The aim of this study was to identify winter wheat lines that combine low levels of head infection and kernel damage with low levels of grain contamination with mycotoxins. Resistance of 27 winter wheat lines (four with resistance gene Fhb1) and cultivars to FHB was evaluated over a three-year (2017–2019) experiment established in two locations (Poznań and Radzików, Poland). At the anthesis stage, heads were inoculated with Fusarium culmorum isolates. The FHB index was scored, and the percentage of Fusarium-damaged kernels (FDKs) was assessed. The grain was analyzed for type B trichothecenes (deoxynivalenol and derivatives and nivalenol) and zearalenone content. The average FHB index of both locations was 12.9%. The proportion of FDK was 6.9% in weight and 8.5% in number. The average content of deoxynivalenol amounted to 3.543 mg/kg, and the average amount of nivalenol was 2.115 mg/kg. In total, we recorded 5.804 m/kg of type B trichothecenes. The zearalenone content in the grain was 0.214 mg/kg. Relationships between the FHB index, FDK, and mycotoxin contents were highly significant for wheat lines; however, these relationships were stronger for FDK than for FHB index. Breeding lines combining all types of FHB resistance were observed, five of which had resistance levels similar to those of wheat lines with the Fhb1 gene.

Fusarium head blight (FHB) can cause contamination of cereal grain with mycotoxins. Triticale is also infected with FHB; however, it is more resistant than wheat to head infection. The aim of this study was to identify triticale lines that combine low head infection with low toxin contamination. Resistance to FHB of 15 winter triticale and three winter wheat lines was evaluated over a three-year experiment established in two locations. At the anthesis stage, heads were inoculated with Fusarium culmorum isolates. The FHB index was scored and the percentage of Fusarium-damaged kernels (FDKs) assessed. The grain was analysed for type B trichothecenes (deoxynivalenol and derivatives, nivalenol) and zearalenone content. The average FHB index was 10.7%. The proportion of FDK was 18.1% (weight) and 21.6% (number). An average content of deoxynivalenol amounted to 7.258 mg/kg and nivalenol to 5.267 mg/kg. In total, it was 12.788 mg/kg of type B trichothecenes. The zearalenone content in the grain was 0.805 mg/kg. Relationships between FHB index, FDK, and mycotoxin contents were statistically significant for triticale lines; however, they were stronger for FDK versus mycotoxins. Triticale lines combing all types of FHB resistance were found, however the most resistant ones were less resistant that wheat lines with the Fhb1 gene.

Shoot and root apical meristems (SAM and RAM, respectively) are crucial to provide cells for growth and organogenesis and therefore need to be maintained throughout the life of a plant. However, plants lacking the mitochondrial protease AtFTSH4 exhibit an intriguing phenotype of precocious cessation of growth at both the shoot and root apices when grown at elevated temperatures. This is due to the accumulation of internal oxidative stress and progressive mitochondria dysfunction. To explore the impacts of the internal oxidative stress on SAM and RAM functioning, we study the expression of selected meristem-specific (STM, CLV3, WOX5) and cell cycle-related (e.g., CYCB1, CYCD3;1) genes at the level of the promoter activity and/or transcript abundance in wild-type and loss-of-function ftsh4-1 mutant plants grown at 30 °C. In addition, we monitor cell cycle progression directly in apical meristems and analyze the responsiveness of SAM and RAM to plant hormones. We show that growth arrest in the ftsh4-1 mutant is caused by cell cycle dysregulation in addition to the loss of stem cell identity. Both the SAM and RAM gradually lose their proliferative activity, but with different timing relative to CYCB1 transcriptional activity (a marker of G2-M transition), which cannot be compensated by exogenous hormones.