The crop root system is pivotal for water and nutrient uptake and environmental stress adaptations. Wheat, as the major calorie provision for the world's population, successfully increases its yield for world population expansion with modern breeding selection. However, the root adaptation in modern wheat cultivars still remain unknown. Here we present the root transcriptomes of 351 wheat accession, which showed a distinct transcriptomic profile between landraces (LA) and modern cultivars (MC), suggesting a significant change of MC in environmental adaptation and root development. The MC seedlings showed a significantly bigger root system, which is mainly contributed by the well-known green revolution allele Rht-D1b. The suppressed GA signaling by Rht-D1b inhibits the cell length in above-ground tissue for a dwarf structure, but increases the cell width in the root meristem, resulting in bigger root diameter and a bigger root volume. This distinct regulation between above- and under-ground contribute a significantly larger root-shoot ratio to modern wheat cultivars. Our data provide new insights for the successful adoption of Rht-D1b and Rht-B1b in green revolution, and the application of Rht-D1b and Rht-B1b in future wheat breeding and production.

Background SLCO4A1-AS1 was found to be upregulated in several cancer types, including colorectal cancer (CRC). However, the detailed roles of SLCO4A1-AS1 in CRC remain to be elucidated. Therefore, we investigated the functions, mechanism, and clinical significance of SLCO4A1-AS1 in colorectal tumourigenesis. Methods We measured the expression of SLCO4A1-AS1 in CRC tissues using qRT-PCR and determined its correlation with patient prognosis. Promoter methylation analyses were used to assess the methylation status of SLCO4A1-AS1. Gain- and loss-of-function assays were used to evaluate the effects of SLCO4A1-AS1 on CRC growth in vitro and in vivo. RNA pull-down, RNA immunoprecipitation, RNA-seq, luciferase reporter and immunohistochemistry assays were performed to identify the molecular mechanism of SLCO4A1-AS1 in CRC. Results SLCO4A1-AS1 was frequently upregulated in CRC tissues based on multiple CRC cohorts and was associated with poor prognoses. Aberrant overexpression of SLCO4A1-AS1 in CRC is partly attributed to the DNA hypomethylation of its promoter. Ectopic SLCO4A1-AS1 expression promoted CRC cell growth, whereas SLCO4A1-AS1 knockdown repressed CRC proliferation both in vitro and in vivo. Mechanistic investigations revealed that SLCO4A1-AS1 functions as a molecular scaffold to strengthen the interaction between Hsp90 and Cdk2, promoting the protein stability of Cdk2. The SLCO4A1-AS1-induced increase in Cdk2 levels activates the c-Myc signalling pathway by promoting the phosphorylation of c-Myc at Ser62, resulting in increased tumour growth. Conclusions Our data demonstrate that SLCO4A1-AS1 acts as an oncogene in CRC by regulating the Hsp90/Cdk2/c-Myc axis, supporting SLCO4A1-AS1 as a potential therapeutic target and prognostic factor for CRC.