Background: Mutations in GJB2 are the most common molecular defects responsible for autosomal recessive nonsyndromic hearing impairment (NSHI). The mutation spectra of this gene vary among different ethnic groups.

BackgroundFlixweed (Descurainia sophia L.) is a troublesome and widespread broadleaf weed in winter fields in China, and has evolved high level resistance to acetolactate synthase (ALS)-inhibiting sulfonylurea herbicide tribenuron-methyl.ResultsWe identified a resistant flixweed population (N11) exhibiting 116.3-fold resistance to tribenuron-methyl relative to the susceptible population (SD8). Target-site ALS gene mutation Pro-197-Thr was identified in resistant plants. Moreover, the resistance can be reversed to 28.7-fold by the cytochrome P450 inhibitor malathion. The RNA-Sequencing was employed to identify candidate genes involved in non-target-site metabolic resistance in this population. Total 26 differentially expressed contigs were identified and eight of them (four P450s, one ABC transporter, three glycosyltransferase) verified by qRT-PCR. Consistent over-expression of the two contigs homology to CYP96A13 and ABCC1 transporter, respectively, were further qRT-PCR validated using additional plants from the resistant and susceptible populations.ConclusionsTribenuron-methyl resistance in flixweed is controlled by target-site ALS mutation and non-target-site based mechanisms. Two genes, CYP96A13 and ABCC1 transporter, could play an important role in metabolic resistance to tribenuron-methyl in the resistant flixweed population and justify further functional studies.Electronic supplementary materialThe online version of this article (doi:10.1186/s12864-016-2915-8) contains supplementary material, which is available to authorized users.

No abstract

No abstract

No abstract