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The Origin of Fruit Ripening

A gaseous plant hormone turns off anti-ripening genes, enabling fruit to mellow--and taste good



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Bananas hanging on a tree or sitting in the produce section of the grocery store start out green, plenty hard and none too tasty. Over time, of course, they become softer and sweeter. The cause of fruit ripening is a natural form of a chemical synthesized to make PVC (polyvinyl chloride) piping and plastic bags—namely, a gaseous plant hormone called ethylene.

For thousands of years, people have used various techniques to boost ethylene production even if they did not quite know it. Ancient Egyptian harvesters slashed open the figs they collected to stimulate ripening, and Chinese farmers would leave pears in closed rooms with incense burning. Later research showed that wounding and high temperatures trigger plants to produce ethylene.

In 1901 Russian scientist Dimitry Neljubow showed that ethylene could affect plant growth after he identified it as the active ingredient in vapors leaking from a gas main. The vapors were causing surrounding plants to grow abnormally. Three decades later, researchers found that plants not only responded to ethylene, but they could produce their own, and production of the gas increased when the scientists cut (injured) the fruit with a knife.

Researchers later discovered that plants produce ethylene in many tissues in response to cues beyond the stress from heat and injury. It is made during certain developmental conditions to signal seeds to germinate, prompt leaves to change colors, and trigger flower petals to die. Because the gas diffuses easily it can travel within the plant from cell to cell as well as to neighboring plants, serving as a warning signal that danger is near and that it is time to activate the appropriate defense responses.

Special receptors in plant cells bind to the ethylene. The first known plant genes involved in this process, ETR1 and CTR1, were identified in 1993; they keep the fruit ripening genes from activating until ethylene is made. Once that happens, ETR1 and CTR1 turn off, which allows a cascade that ultimately turns on other genes that make various enzymes: pectinases to break down cell walls and soften the fruit; amylases to convert carbohydrates into simple sugars; and hydrolases to degrade the chlorophyll content of the fruit resulting in color change. Such changes invite animals to consume the fruit and disperse the mature undigested seeds via their defecation.

The evolution of the ethylene pathway, from the production of the gas to end responses like cell death, still puzzle scientists. Land plants are the only organisms known to contain the entire response system.  Cyanobacteria can sense ethylene, but whether they can produce the compound is unknown. These microorganisms have an ETR1-like gene, but no CTR1 gene, so their ethylene response system would have to be different from that of land plants. Green algae, generally thought to lie between cyanobacteria and land plants in the evolutionary tree, do not perceive ethylene, so how ethylene responses jumped from cyanobacteria directly into land plants also interests researchers.

For economic reasons, scientists continue to explore the biomolecular details of the ethylene production–response cycle, in hopes of developing better methods of preventing fresh-picked fruit from ripening during transport over long distances. The trick is to ensure that the fruit does not become ethylene-insensitive so that it never ripens. After all, who wants to eat green bananas that taste like fiberboard?

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