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Rapeseed is one of the most important oilseeds crops worldwide. Although stem development greatly affects crop yield, its molecular mechanisms remain elusive in rapeseed. This study found a stem bending 1 (stb1) mutant in rapeseed with abnormal stem development and performed phenotype characterization, genetic analysis, quantitative trait locus mapping, and transcriptome analysis. The key stage of stem bending in stb1 mutant occurred at Biologische Bundesanstalt, Bundessortenamt and CHemical industry (BBCH) stages 59–61, from the end of stem elongation to early flowering. The number of vessels and the degree of development of stem xylem, sclerenchyma, and parenchyma cells were extremely lower in stb1 mutant than in elite cultivar ZS11. Genetic analysis revealed that stb1 is controlled by a single recessive locus located between markers Bn-A01-p2421445 and Bn-A01-p4230829 on chromosome A01. Using RNA-seq, identified 1631 genes that differentially expressed between mutant and normal F 2 plants in the shoot apical meristem and stem. The down-regulated genes were mainly overrepresented in auxin transport and coenzyme metabolism processes. Combining data on the auxin concentrations in stem and expression of candidate genes within the mapping interval in the mutant, it was speculated that the phenotype of the stb1 mutant may be caused by defects in polar auxin transport, as two auxin transport-related genes were obviously down-regulated in the mutant. Among them, BnSOS3-INTERACTING PROTEIN3 , which encodes a CBL-interacting protein kinase, was considered the most promising candidate gene for further investigation. These results lay a foundation for better understanding the molecular mechanisms of stem development in rapeseed. • Abnormal stem development of a stem bending 1 (stb1) mutant was found in rapeseed at the BBCH stages 59 to 61. • The stb1 is controlled by a single recessive locus located between markers Bn-A01-p2421445 and Bn-A01-p4230829. • The phenotype of stb1 may be caused by mutation of BnSOS3-INTERACTING PROTEIN3 that controls polar auxin transport. [ABSTRACT FROM AUTHOR]