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The Hindu
2 hours ago
- Science
- The Hindu
How does a plant's first shoot rise safely through soil, into daylight?
Researchers from the Indian Institute of Science Education and Research (IISER), Bhopal, have found that a single protein helps plants time their first step from darkness into light. When a seed sprouts in darkness under the soil, its stem curves into a small hook shape that protects the delicate shoot tip as it pushes upward. The hook needs to stay 'closed' until the seedling breaks through the soil and meets light. In the study, the team wanted to know how two common signals — ethylene, a plant hormone that builds up underground, and light — work together to decide exactly when the hook opens. The team focused on what a gene called BBX32 really does in the model plant Arabidopsis thaliana. By comparing seedlings modified to lack BBX32, to churn out extra copies, to carry extra mutations, or to glow blue or green when the gene was activated or its protein moved around, the scientists could pinpoint how the protein made by the gene helps keep the hook closed. The team also grew seedlings indarkness, red, blue, far-red light, and normal light, in plates with or without a compound that raises ethylene levels, and in thin layers of sand to imitate soil pressure. They photographed three-day-old seedlings and used software to measure the hook angle as it opened over time. They also used genetic tools to track the performance of the BBX32 gene and counted how many seedlings breached a sand layer and turned green. The findings were published in New Phytologiston May 28. The team comprised Nevedha Ravindran, Kavuri Venkateswara Rao, and Sourav Datta of the Department of Biological Sciences at IISER Bhopal. They found that ethylene turns BBX32 on and that light protects BBX32 from being destroyed. The role of BBX32 itself is to keep the hook closed for longer. Without extra ethylene, BBX32 mutants behave like normal plants whereas with high ethylene or a sand cover, the hook opens too soon. BBX32 was found to work by raising the activity of the PIF3 protein, which switched on HLS1, which kept the hook closed. If PIF3 was missing, BBX32 couldn't prevent the hook from opening. In the sand test, only about a quarter of seedlings ever reached the surface compared to 40% of normal seedlings and 80% of over-expressors. Keeping the hook closed just a bit longer clearly helped a sprout survive its climb. The researchers also worked out why BBX32 accumulates only when it's most useful. In total darkness, an enzyme called COP1 latches onto BBX32 and sends it to be degraded, keeping the hook flexible. Ethylene partially shields BBX32, but once the emerging seedling first senses daylight, COP1 activity drops, allowing the protein to build up on the concave side of the hook and hold it shut a little longer. This finely tuned handshake offers a way to breed crops whose seedlings can breach denser soils — a trait that may be valuable as climate change brings heavier rains.
Yahoo
05-03-2025
- Science
- Yahoo
Plant and human immune systems are closer than we think, study finds
Few living things seem to have less in common than plants and animals, but that assumption is being increasingly challenged. Evolution, and the ways in which the kingdom of plants and the kingdom of animals that munch on them have grown up together, leave their traces even after hundreds and hundreds of millions of years. A study published last month in Nature Plants describes shared biochemical pathways involved in vitamin B6 levels that link human neurological health and plant immunity in ways that may teach us how plant immunity works — and how to better treat neurological conditions, like epilepsy, in humans. 'We've always been intrigued by overlap between plants and humans,' study coauthor Pradeep Kachroo, a botany professor at the University of Kentucky, told Salon in a video interview. The last common ancestor of plants and animals was a little single-celled organism that lived around 1.5 billion of years ago. One descendant of our last common ancestor went on to engulf a photosynthetic bacterium, which would then toil away harnessing the power of the sun to fuel this progenitor of all plants. (The common ancestor had earlier engulfed a different bacterium that became the mitochondrion, an organelle that fuels both plant and animal cells). A different descendant of that common ancestor went on to give rise to all animals and fungi. It's like a fairy tale: one brother goes off to found the kingdom of plants, and the other strikes his own bold path to become the first member of the kingdom of animals and fungi. Today, the descendants of those evolutionary royals of old are very different indeed. Typically green, plants generally stay rooted, soaking up solar energy and converting it to chemical energy. The animals, meanwhile, depend on our evolutionary siblings: we either eat vegetation or something else that does, and thus generate our own energy by consuming theirs. Other than the dependence that results in one eating the other, we would seem to have basically nothing in common. Plants use an amino acid called lysine for many things, including as a part of their detection and response to pests. Kachroo's lab was trying to understand what pipecolic acid does and how it functions, and also what role N-hydroxypipecolic acid plays in immunity. As part of this work, Huazhan Liu, Kachroo's postdoctoral scholar and this study's lead researcher, was trying to clarify how the amino acid lysine gets broken down and used in plants. Her subject was Arabidopsis thaliana, a mustard also known as mouse-ear cress, that has been described as a model plant for genome gnalysis. One metabolite, or product, of lysine produced during this process is called pipecolic acid, and another, produced at a later step, is called N-hydroxypipecholic acid. Liu observed that these two amino acids were appearing at different concentrations. Kachroo, speaking from Kentucky, recounted the story to Salon in a video interview while Liu joined the call from China. 'Pipecolic acid was much more abundant than hydroxycholic acid,' Kachroo explained. If one thing (the substrate, in the language of chemical reactions) is being converted to another thing — the product, the amount of the substrate should almost equal to the product. Something couldn't be right. 'I have this much here. I have very little here.' Liu began to wonder if perhaps something else was using pipecolic acid as a substrate, using it up so that there was less left over for the expected production of N-hydroxypipecolic acid. Now, lysine is found in all sorts of organisms, and the way it's catabolized is pretty well-understood in animals. In plants, some of the steps are less well understood. So in a striking act of scientific creativity, Liu turned to the animal kingdom and to human medical science to figure out what was going realized that, while it's not an essential amino acid for us, pipecolic acid is also present in humans. As Liu learned, if you, a human, eat your distant vegetable brethren, you can get a lot of pipecolic acid in your diet: cucumbers, for example, are high in it. You can also consume lysine itself, as it's also found in plants or sold as supplements. Our gut bacteria breaks down that dietary lysine into pipecolic acid, and lysine may also be converted to pipecolic acid by an enzyme already present in the human body. Liu then wondered whether perhaps a similar enzyme exists in plants. She found it, characterized it biochemically, genetically and enzymatically, created plants that made too much of it… and then realized that this enzyme was not, in fact, unknown to science. But in plants, it was called sarcosine oxidase, because it was (incorrectly, as we now know) believed to break down a different chemical, sarcosine. 'We realized it has nothing to do with sarcosine, but it has everything to do with pipecolic acid,' Kachroo told Salon. This is what was using up the missing pipecolic acid, resulting in less N-hydroxypipecolic acid where more was expected. In the plant, then, lysine gets converted to pipecolic acid, and then this enzyme converts it to P6C, or Δ1-piperideine-6-carboxylic acid, yet another step in the lysine catabolism pathway. But P6C is familiar to medical doctors who work with humans, not plants. That's because there is a type of epilepsy that results when a mutation causes the body to increase P6C production until it accumulates in the body. The excessively high neurotransmission that results produces the symptoms we know as epilepsy. This kind of epilepsy is called pyridoxine-dependent epilepsy, because it's treated by giving the patient heavy amounts of vitamin B6, or pyridoxine. The doctors use a form of B6 because it reacts chemically with P6C, taking up the excess P6C. In plants, overly high P6C levels likewise mess with vitamin B6 levels, disrupting the delicate balance of different types of B6 and causing neuropathology in the plants, just as it does in humans. This study sheds light on evolution in two ways: we can see how biochemical pathways common to two entirely separate kingdoms of life, plants and animals, have been largely conserved through our long history apart. And we can see how we have evolved in tandem. Enzymes found in plants (and probably originally acquired by them through horizontal transfer of genes from bacteria: evolution is super messy) and animals have been repurposed to regulate the levels of vitamin B6 — which we humans can't make ourselves but, supplements aside, only get from plants — in very similar ways. 'Why is it that humans 'decided,' over the course of evolution, to build a pathway which is based on a plant diet, to regulate their vitamins which they are, again, getting from a plant diet? Humans do not make vitamins; vitamin B6 we derive from a plant diet. So they are regulating two components which self-regulate each other. Why? It's because you need a balance. Because if you have too [little] of vitamin B6 you cause problems. If you have too much of vitamin B6 you cause problems,' Kachroo told Salon. And yet, vitamin B6 supplements are sold without prescription and without warning at every pharmacy or health food store or grocery, with no regard to the delicate balance by which we naturally regulate the amounts of this vitamin we get from our diets. 'When we are taking these medicines, we're not realizing how much we are consuming,' Kachroo said, mentioning a woman in treatment for epilepsy who approached him in Mexico after he spoke at a conference there. She told him she was taking B vitamins. Indeed, the amount she was taking far exceeded daily requirements — and the Mexican diet already contains ample B6: avocado is one of the richest sources of it. Like plants, which can develop neuropathological problems, becoming susceptible to invasion by pathogens, if their vitamin B levels are too high or too low, a patient like the one with whom Kachroo spoke could be at risk of epileptic symptoms simply because she's supplementing a natural diet with additional B6. It can be risky messing with nature. 'We become,' Kachroo told Salon, 'who we are based on the diet we consume.'
Yahoo
19-02-2025
- Health
- Yahoo
How plants are able to remember stress without a brain
It may sound strange but plants can remember stress. Scientists are still learning about how plants do this without a brain. But with climate change threatening crops around the world, understanding plant stress memory could help food crops become more resilient. Since their colonisation of the land 500 million years ago, plants have evolved ways to defend themselves against pests and disease. One of their most fascinating abilities is to 'remember' stressful encounters and use this memory to defend themselves. This phenomenon, called immune priming, is similar to how vaccines help humans build immunity but is based on different mechanisms. So how do they do it without a brain? Many people think of plants as nice-looking greens. Essential for clean air, yes, but simple organisms. A step change in research is shaking up the way scientists think about plants: they are far more complex and more like us than you might imagine. This blossoming field of science is too delightful to do it justice in one or two stories. This story is part of a series, Plant Curious, exploring scientific studies that challenge the way you view plantlife. Plants are genetically resistant to the vast majority of potentially harmful microbes. However, a small number of microbes have evolved the ability to suppress innate immunity, enabling them to infect organisms and cause disease. This is why vertebrates, including humans, have evolved a mobile immune system that relies on B and T memory cells. These memory cells are activated by exposure to a disease or vaccinations, which helps us become more resistant to recurrent infections. Plants don't have specialised cells to acquire immune memory. Instead, they rely on so-called 'epigenetic' changes within their cells to store information about past attacks and prime their innate immune system. Once primed, plants can resist pests and diseases better – even if they were genetically susceptible to begin with. Research over the past ten to 15 years has shown that repeated and prolonged exposure to pests or diseases can cause long-lasting epigenetic changes to plant DNA without altering the underlying sequence of the DNA. This enables plants to stay in a primed defence state. Immune priming has been reported in different plants species, ranging from short-lived annuals, such as thale cress Arabidopsis thaliana that lives several weeks, to long-living tree species, such as Norway spruce that can live up to 400 years. Immune priming comes at a cost for the plant though, such as reduced growth. So the primed memory is reversible and dwindles over longer periods without stress. However, depending on the strength of the stress stimulus, priming can be lifelong and even be transmitted to following generations. The stronger the stress, the longer plants remember. Plants constantly change the activity of their genes in order to develop and adapt to their environment. Genes can be switched off over prolonged periods of time by epigenetic changes. In plants, these changes most frequently happen at transposons (also known as 'jumping genes') – pieces of DNA that can move within the genome. Transposons are usually inactive because they can cause mutations. But stress changes the epigenetic activity in the plant cell that can partially 'wake them up'. This drives the establishment and maintenance of long-lasting memory in plants. In plants that haven't yet experienced stress, defence genes are mostly inactive to prevent unnecessary and costly immune activity. Lasting epigenetic changes to transposons after recovery from disease can prime defence genes for a faster and stronger activation upon recurrent stress. Although scientists are still uncovering exactly how this works, it is clear that epigenetic changes at these jumping genes play an essential role in helping plants adapt to threats. Plants don't only rely on internal epigenetic memory to improve their resilience against pests and diseases. They can also use their environment to store stress memory. When under attack, plants release chemicals from their roots, attracting helpful microbes that can suppress diseases. If this soil conditioning is strong enough, it can leave a long-lasting 'soil legacy' that can benefit plants of the next generation. Once the soil is conditioned, these helpful microbes stay near plant roots to help the plant fight off diseases. In some plant species, such as maize, scientists have identified the secondary metabolites driving this external stress memory. These are specialised metabolites that are not essential for the cell's primary metabolism. They often play a role in defence or other forms of environmental signalling, such as attracting beneficial microbes or insects. Some of the genes controlling these root chemicals are regulated by stress-responsive epigenetic mechanisms. This indicates that the mechanisms driving internal and external plant memory are interconnected. Understanding how plants store and use stress memories could revolutionise crop protection. Harnessing plants' natural ability to cope with pests and diseases might help us reduce reliance on chemical pesticides and create crops that are better at handling environmental stresses. As we face growing challenges from human-made climate change and rising food demands, this research could offer promising tools to develop more sustainable crop protection schemes. This article is republished from The Conversation under a Creative Commons license. Read the original article. Jurriaan Ton receives funding from UKRI-BBSRC (BB/W015250/1)
