CONSTANS interacts with and antagonizes ABF transcription factors during salt stress under long-day conditions

Abstract

CONSTANS (CO) is a critical regulator of flowering that combines photoperiodic and circadian signals in Arabidopsis (Arabidopsis thaliana). CO is expressed in multiple tissues, including seedling roots and young leaves. However, the roles and underlying mechanisms of CO in modulating physiological processes outside of flowering remain obscure. Here, we show that the expression of CO responds to salinity treatment. CO negatively mediated salinity tolerance under long-day (LD) conditions. Seedlings from co mutants were more tolerant to salinity stress, whereas overexpression of CO resulted in plants with reduced tolerance to salinity stress. Further genetic analyses revealed the negative involvement of GIGANTEA (GI) in salinity tolerance requires a functional CO. Mechanistic analysis demonstrated that CO physically interacts with four critical basic leucine zipper (bZIP) transcription factors; ABSCISIC ACID-RESPONSIVE ELEMENT BINDING FACTOR1 (ABF1), ABF2, ABF3, and ABF4. Disrupting these ABFs made plants hypersensitive to salinity stress, demonstrating that ABFs enhance salinity tolerance. Moreover, ABF mutations largely rescued the salinity-tolerant phenotype of co mutants. CO suppresses the expression of several salinity-responsive genes and influences the transcriptional regulation function of ABF3. Collectively, our results show that the LD-induced CO works antagonistically with ABFs to modulate salinity responses, thus revealing how CO negatively regulates plant adaptation to salinity stress.

Abscisic acid and GIGANTEA signalling converge to regulate the recruitment of CONSTANS to theFTpromoter and activate floral transition

“…Whether this model of interplay between ABFs and NF-YA/B/C/NF-YCO/B/C can be applied to the FT promoter regulation is unclear. Intriguingly, recent data support the physical interaction between CO and ABF1/2/3/4 and their antagonistic roles at salinity-responsive genes promoters (Du et al, 2023). The ABFs do not, however, display binding to the FT chromatin region (Song et al, 2016;Hwang et al, 2019).…”

Comparative transcriptome and coexpression network analysis reveals key pathways and hub candidate genes associated with sunflower (Helianthus annuus L.) drought tolerance

“…This gene is homologous to Arabidopsis thaliana AT1G45249 (Supplementary Table 4 ). In Arabidopsis, this gene encodes abscisic acid response element binding Factor 2, and several studies have reported that this gene is responsive to salt stress [ 122 ] and drought tolerance [ 123 ]. These results reveal the important role of transcription factors in the response to ABA and drought stress in sunflowers.…”

Involvement of CONSTANS-like Proteins in Plant Flowering and Abiotic Stress Response

“…In model plant Arabidopsis, AtCOL4 participates in ABA pathway and salt-stress responses through an ABA-dependent signaling pathway to positively regulate non-biological stress tolerance [149]. Conversely, AtCO negatively mediates salt tolerance in Arabidopsis by interacting with four ABSCISIC ACID-RESPONSIVE ELEMENT BINDING FACTORS (ABF1, ABF2, ABF3, and ABF4) [150]. Additionally, CO is also a JAZ-binding factor that participates in jasmonic acid signal transduction through protein interactions In model plant Arabidopsis, AtCOL4 participates in ABA pathway and salt-stress responses through an ABA-dependent signaling pathway to positively regulate nonbiological stress tolerance [149].…”

“…Additionally, CO is also a JAZ-binding factor that participates in jasmonic acid signal transduction through protein interactions In model plant Arabidopsis, AtCOL4 participates in ABA pathway and salt-stress responses through an ABA-dependent signaling pathway to positively regulate nonbiological stress tolerance [149]. Conversely, AtCO negatively mediates salt tolerance in Arabidopsis by interacting with four ABSCISIC ACID-RESPONSIVE ELEMENT BINDING FACTORS (ABF1, ABF2, ABF3, and ABF4) [150]. Additionally, CO is also a JAZ-binding factor that participates in jasmonic acid signal transduction through protein interactions [151].…”