Osmotic stress represses root growth by modulating the transcriptional regulation of PIN‐FORMED3

Abstract

Osmotic stress influences root system architecture, and polar auxin transport (PAT) is well established to regulate root growth and development. However, how PAT responds to osmotic stress at the molecular level remains poorly understood. In this study, we explored whether and how the auxin efflux carrier PIN-FORMED3 (PIN3) participates in osmotic stress-induced root growth inhibition in Arabidopsis (Arabidopsis thaliana).We observed that osmotic stress induces a HD-ZIP II transcription factor-encoding gene HOMEODOMAIN ARABIDOPSIS THALIANA2 (HAT2) expression in roots. The hat2 loss-offunction mutant is less sensitive to osmotic stress in terms of root meristem growth. Consistent with this phenotype, whereas the auxin response is downregulated in wild-type roots under osmotic stress, the inhibition of auxin response by osmotic stress was alleviated in hat2 roots. Conversely, transgenic lines overexpressing HAT2 (Pro35S::HAT2) had shorter roots and reduced auxin accumulation compared with wild-type plants.PIN3 expression was significantly reduced in the Pro35S::HAT2 lines. We determined that osmotic stress-mediated repression of PIN3 was alleviated in the hat2 mutant because HAT2 normally binds to the promoter of PIN3 and inhibits its expression.Taken together, our data revealed that osmotic stress inhibits root growth via HAT2, which regulates auxin activity by directly repressing PIN3 transcription.

Hydrogen sulfide alleviates osmotic stress‐induced root growth inhibition by promoting auxin homeostasis

“…To explore the role of H 2 S in detail, we then transferred 4-day-old seedlings with 50 lM NaHS, 200 mM mannitol or combination treatments of NaHS and mannitol for continued growth for 3 days and examined the morphological changes of root meristem zone length and root meristem cell number under osmotic stress. Mannitol treatment significantly inhibited both the length and the cell number of root meristem zone in the wild-type, in agreement with a previous study (Yuan et al, 2021) (Figure 2a). However, when co-treated with 50 lM NaHS, the mannitol-mediated inhibition of the root meristem zone could be partly restored, including both the length (Figure 2b,c) and cell number (Figure 2d,e) of the meristem zones, indicating that NaHS is involved in the alleviation of the inhibition.…”

“…H 2 S functions in relieving the inhibition of root meristem development under osmotic stress Reportedly, the osmotic stress-induced reduction in root growth is caused by inhibition of root meristem development in the primary root (Cajero-Sanchez et al, 2019;Rowe et al, 2016;Yuan et al, 2021). To explore the role of H 2 S in detail, we then transferred 4-day-old seedlings with 50 lM NaHS, 200 mM mannitol or combination treatments of NaHS and mannitol for continued growth for 3 days and examined the morphological changes of root meristem zone length and root meristem cell number under osmotic stress.…”

Do Opposites Attract? Auxin-Abscisic Acid Crosstalk: New Perspectives

“…However, the stimuli that induce WRKY41 are not yet clear, and their elucidation might reveal new interactions. PIN3 expression is also directly inhibited by HAT2, an HD-Zip II transcription factor, whose expression is upregulated by osmotic stress, at least in roots, thus inhibiting meristem growth [ 185 ], and its expression is also downregulated in response to NaCl [ 186 ], but the exact mechanism remains uncertain. Auxin-ABA interactions remain particularly understudied in relation to cold responses, which are mediated by ABA [ 187 ].…”

Do Opposites Attract? New Insight into the Crosstalk between Auxin and ABA.

“…However, the stimuli that induce WRKY41 are not yet clear, and their elucidation might reveal new interactions. PIN3 expression is also directly inhibited by HAT2, an HD-Zip II transcription factor, whose expression is up-regulated by osmotic stress at least in roots, thus inhibiting meristem growth [181], and its expression is also down-regulated in response to NaCl [182], but the exact mechanism remains uncertain. Auxin-ABA interactions remain particularly understudied in relation to cold responses, which are mediated by ABA [183].…”