In an exclusive AgroSpectrum interview, Haiyang Liu and Motoki Tominaga of Waseda University unpack their breakthrough discovery that myosin XI-1, a cytoskeletal motor protein, unexpectedly modulates intracellular Na⁺ homeostasis and shapes plant salt tolerance. Their findings suggest that XI-1 influences ion transport indirectly by steering the trafficking and spatial organization of membrane transporters, revealing a novel mechanistic layer in cytoskeleton–ion flux coordination.

The researchers highlight clear sub-functionalization within the Myosin XI family, with XI-1 emerging as a unique regulator whose loss enhances salt resilience but introduces classic trade-offs with growth efficiency. They also outline the translational promise of CRISPR-based fine-tuning of XI-1 in crops like rice and wheat, while cautioning that germination defects in triple knockouts underscore the need for stage-specific deployment. Looking ahead, they emphasize that validating XI-1 function across diverse crop genomes and environments will be the key step before this discovery can enter mainstream breeding pipelines for climate-resilient agriculture.

Molecular Mechanism & Novelty

Your study suggests that Myosin XI-1 modulates intracellular Na⁺ homeostasis, a function previously uncharacterized for motor proteins. Mechanistically, what is the most plausible model explaining how a cytoskeletal motor influences ion transport and compartmentalization under salt stress?

We consider the most plausible explanation to be that Myosin XI may influence intracellular Na⁺ homeostasis by modulating the trafficking and spatial localization of membrane proteins involved in Na⁺ transport. However, at present the evidence is correlative; whether XI-1 acts on a single transporter, multiple transporters, or more generally on trafficking routes remains to be determined and will require direct localization, interaction and functional assays.

Functional Diversification Among Myosin XI Members

Only the AtXI-1 loss-of-function mutant showed enhanced salt tolerance, while AtXI-K and AtXI-2 did not. What does this reveal about sub-functionalization within the Myosin XI family, and are there structural motifs unique to XI-1 that may underpin this divergence?

AtXI-1, AtXI-K, and AtXI-2 share a highly conserved overall domain architecture as members of the Myosin XI family (including the motor domain, IQ motifs, coiled-coil region, and globular tail domain), existing sequence analyses and functional studies indicate that they may differ subtly in regulatory regions within the tail domain, which could contribute to functional specialization.

That said, we cannot yet conclude that XI-K or XI-2 have no role in salt stress responses. Their contributions may be subtle, context-dependent, or masked by genetic redundancy. Functional assays, comparative interactome mapping, domain-swap experiments, and the identification of adaptor proteins that mediate cargo binding will be needed to determine whether structural motifs unique to XI-1 indeed underlie its specific involvement in salt tolerance.

Cytoplasmic Streaming vs. Stress Response Trade-offs

Given Myosin XI’s central role in cytoplasmic streaming and organelle positioning, how do you interpret the evolutionary trade-off between maintaining intracellular trafficking efficiency and developing stress resilience in AtXI-1 mutants?

Given that Myosin XI functions as a central driver of cytoplasmic streaming and organelle positioning, we propose that the enhanced salt tolerance observed in AtXI-1 mutants reflects a typical evolutionary trade-off between maintaining efficient intracellular trafficking and improving stress adaptability.

Under normal growth conditions, XI-1 is responsible for vesicle trafficking, organelle positioning, and the efficient distribution of nutrients and metabolites. Loss of its function somewhat reduces cytoplasmic streaming, slows growth, and thereby diminish competitive fitness. However, under salt stress, the reduced XI-1 activity may alter the spatial distribution of membrane proteins or organelles, thereby limiting cytosolic sodium accumulation and enhancing stress tolerance.

Thus, the salt-tolerant phenotype conferred by the absence of  Myosin XI comes at the cost of growth and transport efficiency under optimal conditions, highlighting a classic “growth–stress tolerance” trade-off: XI-1 supports maximal growth, whereas its loss can provide a conditional advantage under specific stress environments. This explains why XI-1 has been evolutionarily retained rather than eliminated.

Interestingly, single mutations in myosin XI-1, XI-2, or XI-K have little effect on cytoplasmic streaming velocity or plant growth under laboratory conditions, whereas multiple knockouts cause a marked reduction in both streaming and growth. Furthermore, compared with XI-2 and XI-K, XI-1 appears to be only a minor contributor to streaming and growth.

While XI-1 seems to have specifically evolved toward a role in sodium transport, cytoplasmic streaming and growth appear to be supported by complementary mechanisms among multiple myosin XI isoforms, suggesting that essential growth processes are backed up by functional redundancy within the Myosin XI family.

Translational Potential for Salt-Tolerant Breeding

What is the feasibility of integrating XI-1 modulation into major crops (rice, wheat, soybean)? Would CRISPR-based partial knockdowns or tissue-specific promoters be necessary to avoid potential penalties on growth, germination, or reproductive fitness?

The application of XI-1 modulation in major crops appears to be feasible, but the strategy must be carefully designed to avoid compromising plant growth or yield while enhancing salt tolerance. Although it is not yet clear whether weak-function alleles of XI-1 exist in crop germplasm collections, the identification of such natural variants in the future could allow breeders to utilize them through traditional breeding or marker-assisted selection without the need for gene editing.

Overall, XI-1 modulation holds substantial translational potential, but the key challenge lies in achieving an optimal balance between improved stress tolerance and the maintenance of yield. At the current stage, CRISPR-based fine-tuning of XI-1 expression or the use of tissue-specific promoters to spatially restrict its activity represent the most promising approaches for practical application.

Stage-Specific Phenomena in Triple Knockouts

The 3ko mutants show strong vegetative salt tolerance but poor germination under salinity. How do you interpret this stage-specific dichotomy, and what does it imply for deploying XI-1-targeted strategies in real-world breeding programs?

The poor germination of the 3ko mutants under salt stress is likely attributable to intrinsic defects resulting from the complete loss of myosin XI function. For instance, the 3ko mutation may influence cell wall formation and/or other processes critical for seed hydration, which could prevent seeds from efficiently absorbing and retaining water under high osmotic stress, thereby hindering imbibition and successful germination. In contrast, when only a single myosin XI gene is mutated, such defects are greatly reduced. This is consistent with the observation that XI-1 mutant seeds show higher germination rates under salt stress compared with the wild type.

Cross-talk With Known Salt-Response Pathways

Salt tolerance in plants is dominated by SOS, HKT, and NHX pathways. Do you see myosin XI-1 interacting with, stabilizing, or spatially organizing these ion transporters? Are there early indications of signalling cross-talk or cytoskeletal–ion flux coordination?

It is currently difficult to definitively conclude whether XI-1 directly interacts with these ion transporters, but its potential influence on their spatial localization is highly plausible. Previous studies have shown that mutation in SOS3 disrupts arrangement of actin filaments, suggesting that myosins — which function closely with the actin filaments — may also participate in this regulatory mechanism.

Physiological Outcomes & Energy Economy

Your mutant lines show reduced Na⁺ accumulation and higher chlorophyll and proline levels. Does modulating XI-1 alter the plant’s energy budget or oxidative status under stress? Could XI-1-mediated Na⁺ homeostasis have implications for photosynthetic efficiency or ROS detoxification?

We cannot yet determine whether XI-1 directly participates in energy metabolism or redox regulation; however, we consider it more likely that the observed physiological outcomes arise as downstream consequences of improved ionic homeostasis. By reducing cytosolic Na⁺ accumulation, XI-1 perturbation may indirectly lower the energetic cost associated with ion detoxification, thereby allowing more cellular energy to be allocated toward growth and stress adaptation.

Regarding oxidative status, salt-induced ionic toxicity and osmotic imbalance typically trigger substantial ROS production, and thus reduced Na⁺ toxicity would likely diminish ROS generation. Finally, with respect to photosynthetic efficiency, limiting Na⁺ accumulation in leaf tissues may help preserve chloroplast structure and thylakoid membrane integrity, thereby maintaining photosystem activity.

Scaling the Discovery for Climate-Stressed Agriculture

Considering global salinization and the push for climate-resilient crops, what are the next steps for translating this discovery—large-scale phenotyping, gene stacking with known salt-tolerance loci, or exploring XI-1 analogs in halophytes? How soon could this line of research influence commercial cultivar development ?

I believe the next essential step is to evaluate the stability of XI-1–mediated regulation across different genetic backgrounds and environmental conditions. This includes knocking down, CRISPR-editing, or screening natural variants of XI-1 homologs in major crop species such as rice, wheat, and soybean. Multi-location and multi-environment field trials will be required to assess growth performance, yield traits, and physiological responses under salinized conditions.

If XI-1 manipulation consistently enhances salt tolerance in crops without causing adverse effects on yield or overall fitness, this strategy could realistically enter commercial breeding pipelines within near to medium term.

— Suchetana Choudhury (suchetana.choudhuri@agrospectrumindia.com)