The YUCCA enzymes sit at a critical bottleneck in plant hormone metabolism. They are flavin monooxygenases that function as the rate-limiting step in the indole-3-pyruvic acid, or IPA, pathway, converting IPA into indole-3-acetic acid, the principal naturally occurring auxin known as IAA. Because auxin cannot be synthesized efficiently without them, YUCCA genes effectively control how much of this growth-promoting signal a plant can produce at any given moment. Since the first YUCCA genes were characterized in Arabidopsis two decades ago, versions of the family have been identified in rice, apple, soybean, oilseed rape, peach and many other species, and they have repeatedly been linked to organ formation, vascular development, embryogenesis and stress responses. What remained unknown was how this family looks in mango and what its members actually do.

To answer that question, the Guangxi team mined the published mango genome and identified twelve MiYUCCA genes. Phylogenetic analysis, which compares protein sequences to reconstruct evolutionary relationships, sorted the twelve members into five distinct categories, mirroring the subfamily structure seen in other plants. The researchers then scanned the promoter regions upstream of each gene for cis-acting regulatory elements, the short DNA motifs that transcription factors recognize. This analysis revealed a dense array of hormone-responsive elements alongside motifs associated with abiotic stress, suggesting that mango YUCCA genes are positioned to respond to both developmental cues and environmental challenges. Such promoter architecture provides a roadmap for guessing, and then testing, when and where each gene might act.

Expression profiling across mango fruit development delivered the first major clue. Most of the MiYUCCA genes showed their highest abundance during the earliest stages of fruit growth, after which their expression declined sharply or switched off entirely as the fruit matured. This pattern fits neatly with what is known about auxin’s role in early fruit set, when cell division is rapid and high auxin levels help establish the tissues that will later expand and ripen. It also echoes findings in peach, strawberry and grape, where specific YUCCA genes have been tied to auxin biosynthesis during fruit development and ripening. The message from the expression data was clear: the mango YUCCA family is most active precisely when the fruit is being founded, not when it is filling out.

From the twelve candidates, the team selected two closely related members, MiYUCCA10A and MiYUCCA10B, for functional verification. Using Agrobacterium-mediated transformation, they generated transgenic Arabidopsis plants overexpressing each gene, and then extended the work into tomato, a crop species with a very different growth habit and fruit biology. The results were striking. Transgenic plants of both species flowered significantly earlier than their wild-type counterparts, and measurements confirmed that the engineered plants contained elevated levels of IAA, consistent with the introduced YUCCA enzymes actively boosting auxin biosynthesis. Early flowering is a trait of enormous practical interest, because many fruit trees, mango included, have long juvenile phases that delay breeding programs and orchard returns by years.

The stress-resistance results were equally compelling. When the transgenic Arabidopsis and tomato lines were subjected to salt and drought treatments, they tolerated the challenges markedly better than control plants, surviving and growing under conditions that stunted the wild types. This dual function, promoting both development and stress tolerance, is consistent with a growing body of literature showing that auxin is deeply intertwined with abiotic stress signaling. Previous work has shown, for example, that overexpressing Arabidopsis YUCCA6 in poplar and potato confers auxin-overproduction phenotypes along with enhanced tolerance to water deficit, and that activating YUCCA7 in Arabidopsis improves drought resistance. The mango genes now join this list, and they do so in a horticulturally significant species.

But the story was not one of unalloyed benefits. The overexpression lines carried clear reproductive costs. In both transgenic Arabidopsis and tomato, the number of seeds produced was significantly reduced. Arabidopsis pod length was unaffected, but tomato fruit size dropped markedly in the engineered lines. These trade-offs matter. They illustrate a principle that plant biologists have learned repeatedly: hormones as central as auxin cannot simply be cranked up without consequences, because the same signal that accelerates flowering and hardens plants against stress also participates in seed set and fruit expansion. For any future attempt to deploy MiYUCCA10 genes in crop improvement, the challenge will be to capture the flowering and stress benefits while avoiding penalties on yield and fruit quality, perhaps through tissue-specific or inducible promoters rather than constitutive overexpression.

Perhaps the most intriguing mechanistic discovery came from protein interaction experiments. Using yeast two-hybrid assays and bimolecular fluorescence complementation, a technique that reconstitutes a fluorescent protein only when two candidate partners physically meet inside plant cells, the researchers showed that MiYUCCA10A and MiYUCCA10B interact with five mango proteins: MiSVP1, MiSVP2, MiSVP3, MiSVP4 and MiSVP5, all homologs of SHORT VEGETATIVE PHASE, as well as MiFLC, the mango version of FLOWERING LOCUS C. SVP and FLC are central repressors of the floral transition, the genetic switch that converts a vegetative shoot apex into an inflorescence. In Arabidopsis, FLC holds flowering in check until winter cold or other cues remove it, and SVP proteins act with FLC in repressive complexes. Finding auxin biosynthesis enzymes physically associated with these flowering-time repressors suggests a direct biochemical link between hormone production and the floral transition machinery, hinting that MiYUCCA10 proteins may do more than simply raise auxin levels; they may participate in regulatory complexes that decide when a plant commits to flowering.

The study is part of a broader research program at Guangxi University that has systematically dissected mango flowering genes, including earlier work on the CONSTANS family, the SPL transcription factors and the auxin response factor MiARF18A, each of which also produced early-flowering phenotypes when tested in transgenic Arabidopsis. Together these studies are assembling a molecular wiring diagram of how a tropical fruit tree decides to flower, a process that in orchards is governed by season, temperature and tree age. The work was supported by the National Natural Science Foundation of China and Guangxi science and technology funding programs, reflecting regional investment in one of the province’s signature crops.

For the wider research community, the mango YUCCA study delivers three things at once: a complete genomic inventory of a key auxin biosynthesis family in a major tropical fruit, functional proof that two of its members can reprogram flowering time and stress responses in heterologous species, and a physical interaction map connecting auxin synthesis to canonical flowering repressors. The trade-offs observed in fruit size and seed number are a sober reminder that hormone engineering demands precision, but they also sharpen the questions that future experiments must answer. If researchers can find ways to deploy MiYUCCA10A/B activity only where and when it helps, the prospect of mango trees that flower sooner, shrug off drought and salinity, and still bear full-sized fruit moves from speculation toward genuine breeding strategy. In the meantime, the humble mango has offered science a vivid demonstration that a single pair of enzymes can sit at the crossroads of flowering, stress and fruit development all at once.

Subject of Research: Functional characterization of the mango YUCCA auxin biosynthesis gene family and the effects of MiYUCCA10A/B overexpression on flowering, stress tolerance and fruit development

Article Title: Genome-wide analysis of the mango YUCCA family and overexpression of MiYUCCA10A/B confers early flowering and stress tolerance in transgenic Arabidopsis and tomato

Article References: He, Z., Hu, W., Qin, L., Huang, C., Li, R., Xu, F., Xie, F., Luo, C., & He, X. (2026). Genome-wide analysis of the mango YUCCA family and overexpression of MiYUCCA10A/B confers early flowering and stress tolerance in transgenic Arabidopsis and tomato. Plant Cell Reports, 45(10), Article 304. https://doi.org/10.1007/s00299-026-03981-9

Image Credits: AI Generated

DOI: 10.1007/s00299-026-03981-9

Keywords: mango, YUCCA, auxin, IAA biosynthesis, early flowering, salt tolerance, drought tolerance, transgenic plants, Arabidopsis, tomato, MiSVP, FLC

The protein at the center of the story is WD40-REPEAT 5a, or WDR5a, a structural backbone component of the Arabidopsis COMPASS-like complex. This complex is the plant equivalent of a histone methyltransferase assembly first characterized in yeast and animals, and its job is to deposit trimethylation marks on lysine 4 of histone H3, a modification universally associated with active gene transcription. When WDR5a is present and functional, the COMPASS-like complex maintains proper H3K4me3 levels across the genome, keeping thousands of genes in a transcriptionally permissive state. When WDR5a is lost, those marks erode, and genes that depend on them fall silent. Previous work had shown that WDR5a is constantly turned over by the ubiquitin-proteasome system, but the identity of the proteasome subunit responsible for its degradation, and the developmental consequences of that degradation, remained unknown.

To find the missing link, the researchers turned to a classic tool of molecular biology: the yeast two-hybrid screen. By baiting the screen with WDR5a, they pulled out an unexpected partner, REGULATORY PARTICLE AAA-ATPASE 2a, or RPT2a. RPT2a is no ordinary protein; it is one of six AAA-ATPases that form a ring at the entrance of the 26S proteasome’s regulatory particle, unfolding ubiquitinated substrates and threading them into the proteolytic core for destruction. Earlier studies had established that RPT2a is essential for meristem maintenance in Arabidopsis, and that mutations in the gene cause pleiotropic developmental defects, including a characteristic halted-root phenotype. The new finding suggested that at least part of RPT2a’s developmental influence might flow through a specific substrate: WDR5a itself.

The interaction was not a fleeting artifact of the screen. The team confirmed the physical association between RPT2a and WDR5a in plant cells, and then asked what the interaction means functionally. Their experiments showed that RPT2a promotes the degradation of WDR5a through the 26S proteasome pathway. When proteasomal activity is compromised, or when RPT2a function is reduced, WDR5a accumulates. Conversely, the degradation of WDR5a depends on its prior tagging with ubiquitin, the small protein flag that directs substrates to the proteasome. The researchers traced that tagging to a Cullin4-based ubiquitin ligase complex. CUL4, a scaffold protein, partners with the adaptor DNA Damage Binding protein 1A, or DDB1A, to recognize WDR5a and recruit the enzymatic machinery that attaches ubiquitin chains. This CUL4-DDB1A complex, they found, is what targets WDR5a for ubiquitination in vivo.

Perhaps the most technically satisfying part of the study is the mapping of the ubiquitination sites themselves. By analyzing which lysine residues on WDR5a receive ubiquitin marks, the team identified lysine 31 and lysine 211 as the principal targets. These residues sit on exposed surfaces of the WD40 beta-propeller structure, consistent with their accessibility to the CUL4-DDB1A ligase. Mutating these lysines stabilizes the protein, providing direct genetic evidence that they are the functional degradation signals. The finding echoes a striking parallel from human biology: the X-linked mental retardation gene CUL4B was previously shown to target the mammalian WDR5 ortholog for ubiquitylation, regulating neuronal gene expression. The Arabidopsis work suggests that the strategy of controlling H3K4 methylation by destroying a COMPASS scaffold protein is an evolutionarily conserved theme, deployed independently in plants and animals.

With the degradation pathway established, the researchers connected it to the phenotype that matters most to a plant: when it flowers. WDR5a’s influence on H3K4me3 extends to FLOWERING LOCUS C, or FLC, the master floral repressor of Arabidopsis. FLC encodes a transcription factor that binds directly to the chromatin of FLOWERING LOCUS T (FT) and SUPPRESSOR OF OVEREXPRESSION OF CO 1 (SOC1), the two genes whose activation is required for the floral transition. As long as FLC is expressed, FT and SOC1 stay off and the plant remains vegetative. The new study shows that RPT2a-mediated degradation of WDR5a modulates H3K4me3 at FLC and thereby its expression level, establishing an inverse relationship: when WDR5a is degraded and FLC transcription falls, FT and SOC1 rise, and flowering is promoted. When WDR5a is stabilized, FLC stays high, FT and SOC1 stay low, and flowering is delayed.

The genetic evidence supports this model at every node. Plants with reduced RPT2a function accumulate WDR5a, show altered H3K4me3 patterns, misexpress FLC, and display measurable shifts in flowering time under both long-day and short-day conditions. Manipulating WDR5a levels phenocopies the effects, and the expression changes in FT and SOC1 track faithfully with the FLC changes, exactly as expected from the well-characterized FLC-FT/SOC1 regulatory module. In other words, a proteasome subunit once viewed simply as a generic component of the cell’s waste-disposal system turns out to act as a specific, substrate-selective regulator of a developmental switch, funneling protein-turnover information into the epigenetic control of a single decisive gene.

The broader significance of the work lies in what it reveals about how plants integrate proteostasis with chromatin regulation. The 26S proteasome has long been known to shape plant development, with subunit mutants showing defects in meristem maintenance, hormone signaling, and stress responses. But most of those effects were attributed to the wholesale turnover of signaling proteins such as transcription factors and repressors. The new study adds a subtler layer: by degrading a chromatin scaffold, the proteasome can reconfigure the histone modification landscape itself, changing not just the abundance of individual regulators but the accessibility of entire genomic regions. A recent companion study from another group showed that the RPT2a-MET1 axis controls TERMINAL FLOWER1 and inflorescence meristem determinacy, suggesting that RPT2a may act as a hub connecting protein degradation to multiple chromatin systems, from DNA methylation to histone methylation, across diverse developmental contexts.

There are also practical implications. Flowering time is a major determinant of yield in crops, and the COMPASS-like complex has already been implicated in panicle branching and flowering in rice. If the RPT2a-WDR5a-CUL4/DDB1A pathway identified in Arabidopsis is conserved in crop species, it could offer breeders a new set of targets for tuning flowering schedules, whether to escape seasonal stresses, synchronize flowering for hybrid seed production, or adapt varieties to shifting climates. The identification of specific ubiquitination sites on WDR5a is particularly appealing from this perspective, since those residues define a molecular interface that could in principle be modified to alter protein stability without abolishing function.

Many questions remain. What signals trigger the CUL4-DDB1A ligase to attack WDR5a at a given moment? Is the degradation pathway responsive to environmental cues such as photoperiod or temperature, which are the dominant natural inputs to flowering time? And does RPT2a recognize WDR5a directly, or does it simply provide the proteasomal gate through which the ubiquitinated protein passes? Answering these questions will require connecting the biochemical pathway to the circadian and vernalization circuits that plants use to sense the seasons. What is already clear, however, is that the decision to flower is not made solely at the level of gene transcription. It is also made, moment by moment, at the mouth of the proteasome, where a molecular gatekeeper decides how long a chromatin scaffold survives, and with it, how much longer a plant will wait to bloom.

Subject of Research: Proteasome-mediated degradation of the histone H3K4 methyltransferase component WDR5a and its role in regulating flowering time in Arabidopsis

Article Title: RPT2a-mediated degradation of WDR5a regulates flowering time in Arabidopsis

Article References: Liu, J., Liu, Y.-Y., Wu, J., Zhang, Y.-T., Yang, F., Du, Q., & Chen, L.-Y. (2026). RPT2a-mediated degradation of WDR5a regulates flowering time in Arabidopsis. Plant Cell Reports, 45(10), Article 296. https://doi.org/10.1007/s00299-026-03966-8

Image Credits: AI Generated

DOI: 10.1007/s00299-026-03966-8

Keywords: RPT2a, WDR5a, 26S proteasome, COMPASS-like complex, H3K4me3, flowering time, Arabidopsis, FLC, CUL4-DDB1A, ubiquitination, epigenetics, plant development