Mapping QTL for Fusarium head blight resistance in a tunisian-derived durum wheat population

Fusarium head blight (FHB) damage in durum wheat (Triticum turgidum L. var. durum Desf., turgidum) inflicted massive economic losses worldwide. Meanwhile, FHB resistant durum wheat germplasm is extremely limited. ‘Tunisian108’ is a newly identified tetraploid wheat with FHB resistance. However, genomic regions in ‘Tunisian108’ that significantly associated with FHB resistance are yet unclear. Therefore, a population of 171 backcross inbred lines (BC1F7) derived from a cross between ‘Tunisian108’ and a susceptible durum cultivar ‘Ben’ was characterized. Fusarium graminearum (R010, R1267, and R1322) was point inoculated (greenhouse) or spawn inoculated (field) in 2010 and 2011. Disease severity, Fusarium-damaged kernel (FDK) and mycotoxins were measured. Analysis of variance showed significant genotype and genotype by environment effect on all traits. Approximately 8% of the lines in field and 25% of the lines in greenhouse were more resistance than Tunisian108. A framework linkage map of 267 DArt plus 62 SSR markers was developed representing 239 unique loci and covering a total distance of 1887.6 cM. Composite interval mapping revealed nine QTL for FHB severity, four QTL for DON, and four QTL for FDK on seven chromosomes. Two novel QTL, Qfhb.ndsu-3BL and Qfhb.ndsu-2B, were identified for disease severity, explaining 11 and 6% of the phenotypic variation, respectively. Also, a QTL with large effect on severity and a QTL with negative effect on FDK on chromosome 5A were identified. Importantly, a novel region on chromosome 2B was identified with multiple FHB resistance. Validation on these QTL would facilitate the durum wheat resistance breeding

Mutation update for the SATB2 gene

SATB2-associated syndrome (SAS) is an autosomal dominant neurodevelopmental disorder caused by alterations in the SATB2 gene. Here we present a review of published pathogenic variants in the SATB2 gene to date and report 38 novel alterations found in 57 additional previously unreported individuals. Overall, we present a compilation of 120 unique variants identified in 155 unrelated families ranging from single nucleotide coding variants to genomic rearrangements distributed throughout the entire coding region of SATB2. Single nucleotide variants predicted to result in the occurrence of a premature stop codon were the most commonly seen (51/120=42.5%) followed by missense variants (31/120=25.8%). We review the rather limited functional characterization of pathogenic variants and discuss current understanding of the consequences of the different molecular alterations. We present an expansive phenotypic review along with novel genotype-phenotype correlations. Lastly, we discuss current knowledge on animal models and present future prospects. This review should help provide better guidance for the care of individuals diagnosed with SAS