SUMMARY Adaptation to soil is a well-regulated process vital for plant life. AtHB23 is a homeodomain-leucine zipper I transcription factor (TF), previously revealed as crucial for plant survival in front of salinity conditions. We wondered whether this TF has partners to achieve this essential function. A TF cDNA library screening, Y2H, BiFC, and CoIP assays were complemented with expression analyses and phenotypic characterizations of silenced, mutant, overexpressor, and crossed plants in normal and salinity conditions. We revealed that AtHB23, AtPHL1, and AtMYB68 interact with each other, modulating root development and salinity response. The encoding genes coexpress in specific root tissues and developmental stages. In normal conditions, amiR68 silenced plants have less initiated roots, the opposite phenotype to that showed by amiR23 ones. AtMYB68 and AtPHL1 play contrary roles in lateral root elongation. Under salinity, where AtHB23 plays a crucial positive function, AtMYB68 cooperates with it, whereas AtPHL1 obstructs its action impacting survival ability and supporting the complex interaction between AtHB23, AtPHL1, and AtMYB68 in the primary and lateral roots. The root adaptation capability was associated with the amyloplast state. We identified new molecular players that through a complex relationship determine Arabidopsis root architecture and survival ability in salinity conditions.

A complex tissue-specific interplay between the Arabidopsis transcription factors AtMYB68, AtHB23, and AtPHL1 modulates primary and lateral root development and adaptation to salinity