Yanru Hu

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.

Seed germination and post-germination growth are strictly regulated by phytohormones. In Arabidopsis thaliana, jasmonate (JA) and auxin suppress these processes by boosting abscisic acid (ABA) signaling. However, whether there exists a transcriptional switch orchestrating the intricate interplay among these hormones and the underlying molecular mechanisms remain elusive. Herein, we demonstrated that endogenous JA signaling, involving the CORONATINE INSENSITIVE1 (COI1)–JASMONATE ZIM-DOMAIN (JAZ) module and the downstream MYC2, MYC3, and MYC4 transcription factors, potentiates auxin-induced ABA responses. MYC2, MYC3, and MYC4 interact with AUXIN RESPONSE FACTOR10 (ARF10) and ARF16. Consistently, MYC2 and ARF16 synergistically augment ABA signaling-delayed seed germination. Furthermore, MYC2 and MYC4 form a protein complex with ABSCISIC ACID INSENSITIVE5 (ABI5), a master activator of ABA signaling. Genetic analyses suggested that MYC2 positively facilitates ABA responses largely through ABI5. Notably, MYC2 collaborates with ARF16 to enhance the transcriptional activity and protein abundance of ABI5. Intriguingly, MYC2, ARF16, and ABI5 assemble into a ternary complex. Simultaneously disrupting MYC, ARF10/ARF16, and ABI5 renders the seed germination process insensitive to combined JA, auxin, and ABA. Collectively, our findings unveil the MYC–ARF10/ARF16–ABI5 module as a pivotal molecular switch that integrates JA, auxin, and ABA signaling pathways, thereby enabling plants to mount adaptive responses to challenging environmental conditions.

Low-temperature (LT) stress represents a pivotal environmental factor that significantly impacts plant growth, geographical distribution, and agricultural productivity. As sessile organisms, plants have evolved a suite of sophisticated mechanisms to adapt to LT environments, achieving an optimal balance between growth and cold tolerance, a phenomenon termed the growth and tolerance trade-off. This balance is not a passive outcome but rather an active, dynamic, and adaptive decision-making process regulated by a complex molecular network. This review systematically summarizes the molecular mechanisms underlying plant responses to LT and the equilibrium between growth and cold tolerance, with a particular emphasis on LT perception and signal transduction, the suppression of growth and developmental processes, and the regulatory role of hormonal networks. It underscores the central role of hormonal signaling networks in balancing cold tolerance and growth, and also explores potential future applications in this field.

Seed dormancy and germination are crucial processes affecting the propagation and survival of plant populations. These phenomena are precisely regulated through a complex interplay between internal signals, such as plant hormones and environmental cues including light, temperature, moisture, and nutrient availability. Dormancy release and germination initiation are distinct, yet closely associated, processes involving complex transcriptional, translational, and epigenetic changes mediated by intricate regulatory mechanisms. This review comprehensively summarizes the complex regulatory networks governing seed dormancy and germination across different plant species. By integrating physiological, genetic, and molecular biology perspectives, the latest advances in the research on mechanisms regulating seed dormancy and germination are discussed, providing valuable insights for improving seed quality through biotechnology-based breeding strategies and establishing a solid foundation for future research in this field.

Although ethylene and gibberellin (GA) coordinately regulate plant growth, development, and stress responses, the specifics of how ethylene regulates GA signaling are not well understood. In this study, we clarified the molecular mechanism by which ethylene regulates GA signaling in anthocyanin biosynthesis in apple (Malus × domestica): ethylene promotes the ubiquitination and phosphorylation of a DELLA protein, a central regulator of GA signaling. Our findings revealed that ethylene and GA antagonistically regulate anthocyanin biosynthesis, with ethylene impairing the ubiquitination of the DELLA protein REPRESSOR-of-ga1-3-LIKE 2a (MdRGL2a). The F-box protein ETHYLENE-INSENSITIVE 3-BINDING F-BOX PROTEIN 1 (MdEBF1), a key regulator of ethylene signaling, destabilizes MdRGL2a via the 26S proteasome pathway. Conversely, the ethylene-activated protein kinase MITOGEN-ACTIVATED PROTEIN KINASE 7 (MdMPK7) enhances MdRGL2a stability by protecting it from MdEBF1-mediated degradation. Overall, our results demonstrate that ethylene regulates MdRGL2a homeostasis and GA signaling responses by coordinating MdEBF1 and MdMPK7. These insights advance our understanding of the post-translational modifications of DELLA proteins, GA signal transduction, and phytohormone crosstalk in anthocyanin biosynthesis.

Seed germination and postgerminative growth are precisely regulated by multiple signals. In Arabidopsis thaliana, the phytohormone abscisic acid (ABA) suppresses these processes and several circadian clock-associated proteins mediate ABA responses. Nevertheless, whether seed germination is controlled by temporal signals under diurnal conditions remains obscure, as do the associated underlying molecular mechanisms. Here, we found that the germination of wild-type seeds varies with time of release from cold stratification (i.e. transferred to 22 °C) under diurnal conditions upon ABA, salinity, or osmotic stress exposure. Additionally, the evening complex (EC) components EARLY FLOWERING 3 (ELF3), ELF4, and LUX ARRHYTHMO (LUX) attenuate ABA signaling. Notably, time-dependent seed germination relies on these EC components and other core clock proteins. ELF3, ELF4, and LUX physically interact with and act genetically upstream of ABSCISIC ACID INSENSITIVE3 (ABI3) and ABI5, two crucial transcriptional activators of ABA signaling. ELF3, ELF4, and LUX repress the function and accumulation of ABI3 and ABI5. Consistent with these results, ABI3 and ABI5 are essential for the time-based modulation of seed germination. Our findings highlight the critical effects of temporal signals on seed germination and clarify the mechanism through which the EC components antagonize ABI3 and ABI5 to facilitate the crosstalk between the clock and ABA signaling pathways.

Seed size is crucial for crop yield and plant ecological fitness. The phytohormone jasmonate regulates Arabidopsis thaliana seed size, but the underlying molecular mechanisms remain elusive. Here, we established that CORONATINE INSENSITIVE1 (COI1)-mediated jasmonate signaling acts maternally to repress seed growth. Accordingly, jasmonate signaling suppresses the expression of KLUH (KLU), encoding an inducer of integument cell proliferation. KLU regulates the effects of COI1-mediated signaling on seed size. The JASMONATE ZIM-DOMAIN (JAZ) repressors of jasmonate signaling interact with SUPPRESSOR OF DA1-1 (SOD7) and DEVELOPMENT-RELATED PcG TARGET IN THE APEX4 (DPA4), two transcription factors that directly repress KLU. Overexpression of SOD7 largely rescues the seed size phenotype of coi1 mutants and JAZ1-overexpressing JAZ1-ΔJas plants. Furthermore, SOD7 associates with MYC2 and MYC4, two master transcriptional regulators of jasmonate signaling. SOD7 and MYC2 synergistically decrease KLU transcription and inhibit seed growth, while JAZ1 interferes with their transcriptional activities and physical interaction. Notably, jasmonate signaling considerably impacts seed size under salinity stress, primarily through SOD7 and KLU. Collectively, our findings suggest that the JAZ repressors and MYC transcription factors of the jasmonate signaling pathway coordinate with the SOD7/DPA4–KLU pathway to incorporate jasmonate signals into seed development.

Abscisic acid (ABA) suppresses Arabidopsis (Arabidopsis thaliana) seed germination and post-germinative growth. Nitrate stimulates seed germination, but whether it directly regulates ABA signaling and the associated underlying molecular mechanisms remain unknown. Here, we showed that nitrate alleviates the repressive effects of ABA on seed germination independently of the nitric oxide (NO) pathway. Moreover, nitrate attenuates ABA signaling activated by ABSCISIC ACID INSENSITIVE3 (ABI3) and ABI5, two critical transcriptional regulators of the ABA pathway. Mechanistic analyses demonstrated that ABI3 and ABI5 physically interact with the nitrate signaling-related core transcription factor NIN-LIKE PROTEIN 8 (NLP8). After ABA treatment, NLP8 suppresses ABA responses during seed germination without affecting ABA content. Notably, nitrate represses ABA signaling mainly through NLP8. Genetic analyses showed that NLP8 acts upstream of ABI3 and ABI5. Specifically, NLP8 inhibits the transcriptional functions of ABI3 and ABI5, as well as their ABA-induced accumulation. Additionally, NLP8 overexpression largely suppresses the ABA hypersensitivity of mutant plants exhibiting impaired NO biosynthesis or signaling. Collectively, our study reveals that nitrate counteracts the inhibitory effects of ABA signaling on seed germination and provides mechanistic insights into the NLP8–ABI3/ABI5 interactions and their antagonistic relationships in ABA signaling.