Characterization of a Novel Creeping Tartary Buckwheat () Mutant .

Gravity is known as an important environmental factor involved in the regulation of plant architecture. To identify genes related to the gravitropism of Tartary buckwheat, a creeping line was obtained and designated as from the mutant bank by Co-γ ray radiation. Genetic analysis indicated that the creeping phenotype of was attributed to a single recessive locus. As revealed by the horizontal and inverted suspension tests, was completely lacking in shoot negative gravitropism. The creeping growth of occurred at the early seedling stage, which could not be recovered by exogenous heteroauxin, hormodin, α-rhodofix, or gibberellin. Different from the well-organized and equivalent cell elongation of wild type (WT), exhibited dilated, distorted, and abnormally arranged cells in the bending stem. However, no statistical difference of indole-3-acetic acid (IAA) levels was found between the far- and near-ground bending sides in , which suggests that the asymmetric cell elongation of was not induced by auxin gradient. Whereas, showed up-expressed gibberellin-regulated genes by quantitative real-time PCR (qRT-PCR) as well as significantly higher levels of gibberellin, suggesting that gibberellin might be partly involved in the regulation of creeping growth in . RNA sequencing (RNA-seq) identified a number of differentially expressed genes (DEGs) related to gravitropism at stages I (before bending), II (bending), and III (after bending) between WT and . Venn diagram indicated that only was down-expressed at stages I [Log fold change (LogFC): -3.20], II (LogFC: -4.97), and III (LogFC: -1.23) in , compared with WT. Gene sequencing revealed that a fragment deletion occurred in the coding region of , which induced the destruction of a pbH domain in of . qRT-PCR indicated that was extremely down-expressed in at stage II (0.02-fold of WT). Meanwhile, showed the affected expression of lignin- and cellulose-related genes and cumulatively abnormal levels of pectin, lignin, and cellulose. These results demonstrate the possibility that functions as the key gene that could mediate primary cell wall metabolism and get involved in the asymmetric cell elongation regulation of .