Seed germination is the developmental transition in which the metabolically quiescent embryo resumes growth and initiates seedling development (Bewley, 1997; Finch-Savage and Leubner-Metzger, 2006). Dormancy often serves as an adaptive mechanism, preventing germination under unfavorable conditions. Dormancy release is typically triggered by specific environmental cues, such as prolonged storage, optimal temperatures, or light, which reinitiate growth. Seeds perceive environmental signals and integrate them into endogenous signaling pathways through complex phytohormone networks to elicit downstream responses (e.g., dormancy and germination) (Kendall et al., 2011).

Abscisic acid (ABA) and gibberellins (GAs) are considered the main phytohormones regulating germination. In general, ABA suppresses seed germination, while GA promotes it. At the molecular level, this ABA-GA antagonism is modulated by complex transcriptional networks. ABA signaling is mediated by PYRABACTIN RESISTANCE (PYR)/REGULATORY COMPONENT OF ABSCISIC ACID RECEPTOR (RCAR) receptors that recognize the ABA molecule and inhibit 2C protein phosphatases (PP2Cs). This inhibition, in turn, activates SNF1-related kinases 2 (SnRK2s) and downstream transcription factors ABSCISIC ACID INSENSITIVE 3-5 (ABI3-5), which reinforce dormancy by repressing growth-promoting pathways (Park et al., 2009; Ma et al., 2009; Umezawa et al., 2009; Cutler et al., 2010). As dormancy is released, the expression of ABA biosynthetic genes declines, while catabolic genes, such as cytochrome P450 monooxygenase CYP707A, are upregulated, thereby reducing ABA levels (Okamoto et al., 2006). Concurrently, GA biosynthetic genes, including GA 20-oxidases (GA20ox) and GA3ox, are transcriptionally induced, leading to an increase in bioactive GA levels (Yamaguchi et al., 1998; Seo et al., 2006). Elevated GA levels trigger the proteasomal degradation of DELLA repressors, notably REPRESSOR OF GA1-3-LIKE2 (RGL2), lifting transcriptional constraints on germination-associated genes and enabling radicle protrusion (Dill et al., 2004; Tyler et al., 2004; Piskurewicz et al., 2008).

Auxin, primarily indole-3-acetic acid (IAA), is an important but complex regulator of seed germination (Wang et al., 2011; Liu et al., 2013; Wang et al., 2016; Ye et al., 2016; Shuai et al., 2017; Hussain et al., 2020; Mei et al., 2023; Tognacca et al., 2024). In Arabidopsis thaliana, IAA is produced mainly via the indole-3-pyruvic acid (IPyA) pathway in which TRYPTOPHAN AMINOTRANSFERASE OF ARABIDOPSIS (TAA) and YUCCA (YUC) flavin-containing monooxygenases convert tryptophan to IAA (Casanova-Sáez et al., 2021). Auxin distribution is shaped by polar transport: PIN-FORMED (PIN) efflux and AUXIN1/LIKE-AUX1 (AUX1/LAX) influx carriers establish auxin gradients that guide cell expansion and division (Luschnig and Friml, 2024). Auxin perception proceeds through both intracellular and extracellular routes (Vanneste et al., 2025). Canonically, auxin binding to TRANSPORT INHIBITOR RESPONSE1 (TIR1)/AUXIN-SIGNALING F-BOX (AFB) receptors promotes degradation of Aux/IAA repressors, releasing AUXIN RESPONSE FACTORS (ARFs) to activate transcription (Gray et al., 2001; Kepinski and Leyser, 2005; Tan et al., 2007). Several ARFs are further downregulated post-transcriptionally by microRNAs (miRNAs), refining auxin outputs (Liu et al., 2007).

Although many studies have probed how IAA interacts with the antagonistic balance between ABA and GA, the seed‐specific mechanisms by which auxin regulates germination have not been comprehensively determined. In this mini-review, we synthesize recent advances on auxin’s role in seed germination and its intricate crosstalk with other phytohormones, highlighting key mechanistic nodes and open questions that will direct future investigations.

Auxin biosynthesis is rapidly induced upon fertilization of the central cell, driving early endosperm proliferation (Figueiredo et al., 2015; Batista et al., 2019; Guo et al., 2022). As development proceeds, auxin signaling intensifies during later stages of seed maturation (Pellizzaro et al., 2020). Auxin input and output reporters reveal that auxin response maxima emerge at the funiculus, chalaza, and micropylar integument. These maxima are established through localized TAA1-YUC biosynthesis in specific seed-coat domains and directed transport via PIN3 and AUX1 (Liu et al., 2023). These dynamics reflect coordinated changes in auxin supply, transport, and tissue sensitivity. Auxin signaling during development is associated with increased seed longevity (Pellizzaro et al., 2020) and, when elevated in the seed coat, larger seed size (Liu et al., 2023). Conversely, higher auxin activity in mature seeds is consistent with the maintenance of dormancy and delayed germination.

Early evidence that auxin modulates germination came from exogenous applications of auxinic herbicides, which frequently delayed or inhibited seed germination, establishing that auxin-like activity can influence the germination process (Hamner et al., 1946; Hsueh and Lou, 1947). Subsequent work confirmed that high doses of exogenous IAA or its synthetic analogues delay germination in several species (Ramaih et al., 2003; Liu et al., 2013; Shuai et al., 2017). However, the underlying mechanisms are species-dependent. In Arabidopsis and soybean, inhibition is associated with the shifts in the ABA/GA balance. Exogenous IAA application upregulates ABA biosynthesis and signaling, limits ABA inactivation, while repressing GA biosynthesis and signaling (Liu et al., 2013; Shuai et al., 2017). For tobacco, soaking seeds in high IAA doses reduces the germination speed and can even induce secondary dormancy. In this case, the exogenous application of IAA does not alter ABA content, but instead, increases GA content, which the authors interpret as a compensatory response to counteract the auxin effect. Seeds then recover from dormancy as auxin levels subsequently decline (Li et al., 2016).

In contrast, low doses of IAA can promote seed germination in Arabidopsis (Wang et al., 2016). Seed priming with IAA has been shown to be beneficial in particular species, including cotton and Chinese fir, where it improves germination and seedling growth (Zhao and Zhong, 2013; Zhao et al., 2020), However, this effect was not observed in Arabidopsis (Ye et al., 2016). Auxin treatments can also counteract germination delays caused by salinity or drought in a dose-dependent manner (Ashraf and Foolad, 2005; Iqbal and Ashraf, 2007; Xing et al., 2023; Ellouzi et al., 2024). Consistent with these low-auxin effects, low amounts of IAA synthesized by plant growth-promoting rhizobacteria can also promote seed germination, enhance stress tolerance, and improve nutrient uptake (Fiodor et al., 2023; Shaffique et al., 2023).

Thus, auxin’s effect on seed germination can be either inhibitory or beneficial, depending on the dose, species, and physiological context.

Exogenous application of auxin alters germination in Arabidopsis, and lines overexpressing the iaaM gene, which encodes a bacterial enzyme that increases auxin production, also show severely delayed germination and deep primary dormancy. This observation suggests that perturbations in endogenous IAA can influence germination kinetics, and in turn raises the question of which steps in auxin metabolism are most crucial for seed germination. Disruption of the biosynthetic IPyA pathway, as seen in the yuc1 yuc6 mutant, reduces auxin levels and leads to decreased dormancy and accelerated germination relative to the wild-type (Liu et al., 2013).

At the receptor level, loss of TIR1/AFB impairs Aux/IAA degradation and results in reduced auxin signaling. Loss-of-function tir1, tir1 afb2, tir1 afb3, and tir1 afb1 afb2 afb3 mutants show an enhanced germination rate compared to wild-type, with the most substantial effect in the quadruple mutant under ABA supplementation (Liu et al., 2013). Auxin signaling provides another regulatory layer. Several Aux/IAA genes (IAA1, IAA2, IAA3, IAA16, IAA20, IAA26, IAA28, and IAA29) are highly expressed during germination (Winter et al., 2007; Carranco et al., 2010), suggesting functional relevance. Consistent with this, the loss-of-function iaa8–1 mutant shows delayed radicle protrusion (Hussain et al., 2020). Conversely, gain-of-function mutants axr2-1 (IAA7) and axr3-1 (IAA17) carry mutations that reduce auxin-induced Aux/IAA protein degradation and germinate faster compared to wild-type. Mutants of downstream transcription factors, arf10, arf16, and the arf10 arf16 double mutant, have enhanced germination and display ABA hyposensitivity compared to wild-type. In contrast, transgenic lines expressing miR160-resistant forms of ARF10 and ARF16 have the opposite effect (Liu et al., 2013).

Auxin transporters are also upregulated in non-dormant seeds compared to dormant ones, suggesting that, besides seed development, auxin redistribution plays a role in seed germination (Carrera et al., 2008). The loss-of-function aux1–21 and aux1–22 mutants exhibit slower germination compared to wild-type seeds (Wang et al., 2016). Under ABA treatment, germination is inhibited in both wild-type and pin3-3, pin3-4, aux1-1, pin7-1, pin7–2 mutant seeds. However, mutants in auxin transport show significantly stronger inhibition compared to wild-type (Tognacca et al., 2024), underscoring the role of AUX1/PIN-mediated auxin fluxes in seed germination.

Together, these findings demonstrate that auxin influences germination through multiple regulatory layers, spanning biosynthesis, signaling, and transport (Table 1). Reduced auxin supply or impaired signaling often weakens dormancy, whereas elevated auxin levels reinforce it. Optimal spatial distribution of auxin, mediated by AUX1 and PIN transporters, further fine-tunes the timing of radicle emergence. This multilayered regulation sets the stage for understanding how auxin integrates with ABA and GA signals to control seed germination.

Germination succeeds when the growing embryo generates enough force to overcome the mechanical resistance of the testa and micropylar endosperm. GA promotes the embryo’s growth potential and endosperm loosening, whereas ABA reinforces restraint. Consequently, the spatial distribution of hormones across the embryo and endosperm is critical to timing radicle emergence (Chandrasekaran et al., 2022; Zhao et al., 2022; Matilla, 2025). There is increasing evidence that auxin distribution within the embryo influences germination. At the transcriptional level, GA upregulates, while ABA downregulates the expression of auxin transporters PIN3, PIN7, and AUX1 (Ogawa et al., 2003; Nakabayashi et al., 2005; Penfield et al., 2006). Functionally, chemical inhibition of polar auxin transport or loss-of-function mutations in aux1, pin3, or pin7 slow germination and increase ABA sensitivity (Tognacca et al., 2024). During imbibition, ABA levels decline, whereas IAA often rises under germination-promoting conditions, such as red light (Preston et al., 2009; Tognacca et al., 2024). Accordingly, directed auxin transport must redistribute IAA within the seed compartments. AUX1 facilitates auxin delivery to the radicle tip, and seed-specific AUX1 overexpression increases radicle tip cell number and accelerates germination compared with wild-type (Wang et al., 2016). Consistent with this, Tognacca et al. (2024) proposed that red-light induction of AUX1, PIN3, and PIN7 enhances auxin delivery toward the radicle tip, helping establish a permissive auxin gradient across the embryonic-axis elongation zone and thereby facilitating radicle emergence. Thus, the precise routing of IAA within embryonic tissues is a modulatory step in seed germination, cooperating with GA to enhance embryo growth potential while counteracting the restraint imposed by ABA.

Auxin’s effect on seed germination is both dose- and context-dependent. In Arabidopsis, high auxin concentrations generally delay germination, while low exogenous doses can promote it. Elevated IAA supply via the IPyA pathway increases ARF-dependent transcription and reinforces ABA-dependent dormancy. Whether alternative auxin biosynthetic routes exert similar effects in seeds remains unknown and warrants further investigation.

At the signaling level, ARF functions are dual: ARF10/16 strengthen dormancy by acting through ABI transcription factors and, via crosstalk with JA, assemble an ARF10/16-JAZ-ABI5 regulatory node. In contrast, ARF2 tends to alleviate ABA-mediated inhibition, enabling radicle protrusion. While auxin clearly modifies GA levels in germinating seeds, whether it directly targets GA signaling components remains unclear. In non-seed contexts, Aux/IAA-ARF modules can condition DELLA turnover. Whether analogous seed-specific ARF-DELLA links operate requires demonstration. A plausible, and not mutually exclusive, alternative is that apparent IAA-GA interactions in seeds act indirectly through auxin’s reinforcement of ABA signaling and the established ABA-GA feedback circuitry.

Beyond total hormone levels, AUX1/PIN-mediated auxin routing helps set the timing of radicle protrusion. Local auxin distribution and its interplay with ABA and GA across the embryonic axis and micropylar endosperm likely predict emergence more accurately than bulk hormone levels. This highlights the need for building spatiotemporal maps of IAA, GA, and ABA at cellular resolution to determine when, where, and how much of each phytohormone signal is required to overcome endosperm resistance. Given that auxin can affect germination via biosynthesis, signaling, and transport pathways, it is also reasonable to ask whether auxin inactivation and catabolism tune the kinetics of radicle emergence.

Clarifying how auxin integrates with ABA and GA during germination will enhance our understanding of the dormancy-germination switch and facilitate the development of practical methods to control germination timing and uniformity in agriculturally important crops.