A gibberellin‑responsive MYB transcription factor controls internal browning in pineapple

Pineapples are among the world's most traded tropical fruits, yet they carry a hidden flaw that can turn a perfect-looking purchase into a disappointing experience. Inside the fruit, near the core, the flesh can turn translucent and brown, a condition known as internal browning. Because this damage happens deep within the fruit with no warning signs on the outside, consumers often discover it only after taking a bite, leading to significant waste and financial loss for growers. For decades, scientists believed this browning was primarily caused by the fruit getting too cold. The prevailing theory was that low temperatures damaged the delicate membranes inside the fruit cells, causing enzymes to leak out and react with other chemicals to create brown pigments. While cold storage is a common way to keep fruit fresh, this explanation left some puzzles unsolved, such as why pineapples treated with gibberellin—a natural plant hormone used to help fruit grow—would turn brown even when kept at normal room temperatures.

A team of researchers from the Guangdong Academy of Agricultural Sciences has now uncovered a different story, one that looks less at physical damage and more at the fruit's internal clock and chemical signals. By studying the genetic activity inside pineapples as they began to brown, the scientists identified a specific master switch, a protein called AcMYB108, that drives the browning process. They found that this protein acts like a conductor, turning on a chain reaction of other proteins that eventually break down the fruit's cells, leading to the brown discoloration. Crucially, the study reveals that gibberellin, the hormone often used in farming, accelerates this process by flipping the switch on this master protein and simultaneously disabling a natural brake that usually stops the reaction. This discovery shifts the understanding of internal browning from a simple case of cold-induced injury to a complex biological program linked to how ripe the fruit is and what hormones it encounters.

To solve the mystery, the researchers started by comparing the genetic activity in pineapples that were browning against those that remained healthy. They looked at the fruit pulp at the very moment the browning symptoms appeared. The genetic data showed a clear pattern: the browning fruit had switched on thousands of genes associated with aging and cell death, while the healthy fruit did not. Among the most active genes was AcMYB108. This gene produces a transcription factor, a type of protein that controls which other genes are turned on or off. The researchers observed that the levels of this protein rose sharply just as the browning began, suggesting it was a key player in the disorder. To confirm its role, they introduced extra copies of the AcMYB108 gene directly into pineapple fruit using a harmless bacterium. The result was immediate and dramatic: the fruit injected with the extra gene turned brown much faster and more severely than the control fruit, proving that high levels of this protein are enough to trigger the browning process.

The next step was to figure out how AcMYB108 causes the fruit to rot. The team traced its path by looking for the genes it directly controls. They found that AcMYB108 binds to the DNA of two other proteins, AcWRKY31 and AcWRKY75, and forces them to become active. These two proteins, in turn, activate a third protein called AcSAG12. This final protein is a cysteine protease, an enzyme that acts like a pair of molecular scissors, cutting up the cell's internal structures. When this cascade of events is triggered, the cells break down, leading to the translucent, brown appearance of the fruit. The researchers confirmed this chain of command by showing that AcMYB108 physically attaches to the DNA of the WRKY genes and that the WRKY proteins attach to the DNA of the SAG12 gene. This creates a clear line of command: the master switch turns on the middle managers, who then order the cleanup crew to dismantle the cell.

The study also explains why gibberellin makes the problem worse. Farmers sometimes use gibberellin to improve the size and appearance of pineapples before harvest, but this practice is known to increase the risk of internal browning. The researchers discovered that gibberellin attacks the system from two angles. First, it directly increases the production of the AcMYB108 master switch, flooding the fruit with the signal to start browning. Second, gibberellin interferes with a natural safety mechanism. Inside the cell, a protein called AcDELLA usually binds to AcWRKY75 and stops it from working, acting as a brake on the browning process. However, when gibberellin is present, it causes the AcDELLA brake to be destroyed, freeing AcWRKY75 to do its job. This dual action—turning up the volume on the signal and removing the brake—ensures that the browning process runs unchecked, even if the fruit is kept at a comfortable temperature.

This new understanding challenges the old idea that internal browning is solely a result of cold damage. While cold storage can still trigger the process, the research shows that the fruit's own developmental stage and hormonal balance are equally critical. The study suggests that fruit harvested at a later, riper stage is more susceptible because its internal systems are already closer to the point of no return, making it easier for the AcMYB108 cascade to start. Conversely, fruit harvested earlier might resist the process longer. The findings provide a clear molecular map of how a fruit decides to age and deteriorate. By identifying the specific genes and proteins involved, the research offers a new way to think about preventing these losses. Instead of just focusing on temperature control, growers and scientists can now look at managing the hormonal environment and the timing of the harvest to keep the internal browning genes switched off, potentially extending the shelf life of this popular tropical fruit.