Arabidopsis transcription factor STOP1 directly activates expression of NOD26-LIKE MAJOR INTRINSIC PROTEIN5;1, and is involved in the regulation of tolerance to low-boron stress.

This article focuses on the role of the C2H2-type transcription factor SENSITIVE TO PROTON RHIZOTOXICITY1 (STOP1) in enhancing Arabidopsis tolerance to low-boron (B) stress. The study demonstrates that STOP1 directly binds to the 5´-untranslated region of the boric acid-channel protein gene NOD26-LIKE MAJOR INTRINSIC PROTEIN5;1 (NIP5;1), activating its expression and thereby increasing boron uptake by roots under low-B conditions. Overexpression of STOP1 leads to higher NIP5;1 transcript levels, improved boron uptake, and enhanced plant growth in boron-deficient environments, while genetic analyses confirm that STOP1 and NIP5;1 function in the same pathway for low-B tolerance. These findings identify the STOP1–NIP5;1 regulatory module as a key mechanism for plant adaptation to boron deficiency and suggest its potential application in improving crop tolerance to low-boron soils.