Jingwen Ye

Seed germination is profoundly influenced by diverse environmental stimuli (eg temperatures), but the associated underlying molecular mechanisms remain largely uncharacterized. In this study, we demonstrated that low ambient temperatures, such as 16 °C, suppress Arabidopsis thaliana seed germination, with endogenous abscisic acid (ABA) signaling revealed as a critical part of the underlying mechanism. The germination suppression and ABA response regulation by low ambient temperatures require ABSCISIC ACID INSENSITIVE3 (ABI3) and ABI5, 2 indispensable transcriptional activators in the ABA signaling pathway. In-depth analyses demonstrated physical associations between ABI3/ABI5 and low-temperature-responsive C-REPEAT BINDING FACTOR1 (CBF1), CBF2, and CBF3 (ie CBFs). Genetic evidence confirms that CBFs are essential for low-temperature- and ABA-mediated germination repression. Furthermore, CBFs and ABI3/ABI5 synergistically mediate the inhibitory effects of both low temperatures and ABA on germination. Mechanistically, these factors reciprocally enhance each other's transcriptional activities and promoter enrichment at downstream target genes. Notably, CBFs also directly bind INDUCER OF CBF EXPRESSION1 (ICE1), establishing an antagonistic regulatory axis with ABI5. Collectively, our findings underscore the critical modulatory effects of low ambient temperatures on ABA signaling and seed germination, thereby elucidating the mechanism by which the CBFs–ABI3/ABI5–ICE1 module functions as a signal transducer that converts environmental stimuli into endogenous hormone signals.

Abscisic acid (ABA) represses seed germination and postgerminative growth in Arabidopsis thaliana. Auxin and jasmonic acid (JA) stimulate ABA function; however, the possible synergistic effects of auxin and JA on ABA signaling and the underlying molecular mechanisms remain elusive. Here, we show that exogenous auxin works synergistically with JA to enhance the ABA-induced delay of seed germination. Auxin biosynthesis, perception, and signaling are crucial for JA-promoted ABA responses. The auxin-dependent transcription factors AUXIN RESPONSE FACTOR10 (ARF10) and ARF16 interact with JASMONATE ZIM-DOMAIN (JAZ) repressors of JA signaling. ARF10 and ARF16 positively mediate JA-increased ABA responses, and overaccumulation of ARF16 partially restores the hyposensitive phenotype of JAZ-accumulating plants defective in JA signaling in response to combined ABA and JA treatment. Furthermore, ARF10 and ARF16 physically associate with ABSCISIC ACID INSENSITIVE5 (ABI5), a critical regulator of ABA signaling, and the ability of ARF16 to stimulate JA-mediated ABA responses is mainly dependent on ABI5. ARF10 and ARF16 activate the transcriptional function of ABI5, whereas JAZ repressors antagonize their effects. Collectively, our results demonstrate that auxin contributes to the synergetic modulation of JA on ABA signaling, and explain the mechanism by which ARF10/16 coordinate with JAZ and ABI5 to integrate the auxin, JA, and ABA signaling pathways.

CONSTANS (CO) is a master flowering-time regulator that integrates photoperiodic and circadian signals in Arabidopsis thaliana. CO is expressed in multiple tissues, including young leaves and seedling roots, but little is known about the roles and underlying mechanisms of CO in mediating physiological responses other than flowering. Here, we show that CO expression is responsive to jasmonate. CO negatively modulated jasmonate-imposed root-growth inhibition and anthocyanin accumulation. Seedlings from co mutants were more sensitive to jasmonate, whereas overexpression of CO resulted in plants with reduced sensitivity to jasmonate. Moreover, CO mediated the diurnal gating of several jasmonate-responsive genes under long-day conditions. We demonstrate that CO interacts with JASMONATE ZIM-DOMAIN (JAZ) repressors of jasmonate signaling. Genetic analyses indicated that CO functions in a CORONATINE INSENSITIVE1 (COI1)-dependent manner to modulate jasmonate responses. Furthermore, CO physically associated with the basic helix-loop-helix (bHLH) subgroup IIId transcription factors bHLH3 and bHLH17. CO acted cooperatively with bHLH17 in suppressing jasmonate signaling, but JAZ proteins interfered with their transcriptional functions and physical interaction. Collectively, our results reveal the crucial regulatory effects of CO on mediating jasmonate responses and explain the mechanism by which CO works together with JAZ and bHLH subgroup IIId factors to fine-tune jasmonate signaling.