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 一笈壽司春酒場面夠體面嗎？》台中公益路必吃清單｜10家熱門餐廳完整評測 |
| 心情隨筆｜心情日記 2026/04/19 20:10:22 | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
身為一個熱愛美食、喜歡在城市裡挖掘驚喜的人，臺中公益路一直是我最常出沒的地方之一。這條路可說是「臺中人的美食戰場」，從精緻西餐到創意火鍋，從日式丼飯到義式早午餐，每走幾步，就會有完全不同的特色料理餐廳。 這次我特別花了一整個月，實際造訪了公益路上十間口碑不錯的餐廳。有的是網友熱推的打卡名店，也有隱藏在巷弄裡的小驚喜。我以環境氛圍、口味表現、價格CP值與再訪意願為基準，整理出這篇實測評比。希望能幫正在猶豫去哪裡吃飯的你，找到那一間「吃完會想再來」的餐廳。 評比標準與整理方向
這次我走訪的10家餐廳橫跨不同料理類型，從高質感牛排館到巷弄系早午餐，每一間都有自己獨特的風格。為了讓整體比較更客觀，我依照以下四大面向進行評比，並搭配實際用餐體驗來打分。
整體而言，我希望這份評比不只是「哪家好吃」，而是幫你在不同情境下（約會、家庭聚餐、朋友小聚、商業午餐）都能快速找到合適的選擇。畢竟，美食不只是味覺的滿足，更是一段段與朋友共享的生活記憶。 10間臺中公益路餐廳評比懶人包公益路向來是臺中人聚餐的首選地段，從火鍋、燒肉到中式料理與早午餐，每走幾步就有驚喜。以下是我實際造訪過的10間代表性餐廳清單，橫跨平價、創意、高級各路風格。
一頭牛日式燒肉｜炭香濃郁的和牛饗宴，約會聚餐首選
走在公益路上，很難不被 一頭牛日式燒肉 的木質外觀吸引。低調卻不失質感的門面，搭配昏黃燈光與暖色調的內裝，讓人一進門就感受到濃濃的日式職人氛圍。店內空間不大，但桌距規劃得宜，每桌皆設有獨立排煙設備，烤肉時完全不怕滿身油煙味。 餐點特色
一頭牛的靈魂，絕對是他們招牌的「三國和牛拼盤」。 用餐體驗整體節奏掌握得非常好。店員會在你剛想烤下一片肉時貼心遞上夾子、幫忙換烤網，讓人完全不用分心。整場用餐過程就像一場表演，從視覺、嗅覺到味覺都被滿足。 綜合評分
地址：408臺中市南屯區公益路二段162號電話：04-23206800 小結語一頭牛日式燒肉不僅是「吃肉的地方」，更像是一場五感盛宴。從進門那一刻到最後一道甜點，都能感受到他們對細節的用心。 TANG Zhan 湯棧｜文青系火鍋代表，麻香湯底與視覺美感並重
在公益路這條美食戰線上，TANG Zhan 湯棧 是讓人一眼就會想走進去的那一種。 餐點特色
湯棧最有名的當然是它的「麻香鍋」。 用餐體驗整體氛圍比一般火鍋店更有質感。 綜合評分
地址：408臺中市南屯區公益路二段248號電話：04-22580617 官網：https://www.facebook.com/TangZhan.tw/ 小結語TANG Zhan 湯棧 把傳統火鍋做出新的樣貌保留臺式鍋物的溫度，又結合現代風格與細節服務，讓吃鍋這件事變得更有品味。 如果你想找一間兼具「好吃、好拍、好放鬆」的火鍋店，湯棧會是公益路上最有風格的選擇之一。 NINI 尼尼臺中店｜明亮寬敞的義式早午餐天堂
如果說前兩間是肉食愛好者的天堂，那 NINI 尼尼臺中店 絕對是想放鬆、聊聊天的好地方。餐廳外觀以白色系與大片玻璃窗為主，陽光灑進室內，讓人一踏入就有種度假般的輕盈感。假日早午餐時段特別熱鬧，建議提早訂位。 餐點特色
NINI 的菜單融合義式與臺灣人口味，選擇多樣且份量十足。主打的 松露燉飯 濃郁卻不膩口，米芯保留微Q口感；而 香蒜海鮮義大利麵 則以新鮮白蝦、花枝與淡菜搭配微辣蒜香，口感層次豐富。 用餐體驗店內氣氛輕鬆不拘謹，無論是一個人帶電腦工作、或朋友聚餐，都能找到舒服角落。餐點上桌速度穩定，服務人員態度親切、補水與收盤都非常主動。整體節奏讓人覺得「時間變慢了」，很適合想遠離忙碌日常的人。 綜合評分
地址：40861臺中市南屯區公益路二段18號電話：04-23288498 小結語NINI 尼尼臺中店是一間能讓人放下手機、慢慢吃飯的餐廳。餐點不追求浮誇，而是以「剛剛好」的份量與風味，陪伴每個平凡午後。如果你在找一間能邊吃邊聊天、拍照也漂亮的早午餐店，NINI 會是你在公益路上最不費力的幸福選擇。 加分100%浜中特選昆布鍋物｜平價卻用心的湯頭系火鍋，家庭聚餐好選擇
在公益路這條高質感餐廳林立的戰場上，加分100%浜中特選昆布鍋物 走的是截然不同的路線。它沒有浮誇的裝潢、也沒有高價位的套餐，但靠著實在的湯頭與親切的服務，默默吸引許多回頭客。每到用餐時間，總能看到家庭或情侶三兩成群地圍著鍋邊聊天。 餐點特色
主打 北海道浜中昆布湯底，湯頭清澈卻不單薄，越煮越能喝出海藻與柴魚的自然香氣。 用餐體驗整體氛圍偏家庭取向，桌距寬敞、座位舒適，帶小孩來也不覺擁擠。店員態度親切，補湯、收盤都很勤快，給人一種「被照顧著」的安心感。 綜合評分
地址：403臺中市西區公益路288號電話：0910855180 小結語加分100%浜中特選昆布鍋物是一間「不浮誇、但會讓人想再訪」的火鍋店。它不追求豪華擺盤，而是用最簡單的湯頭與新鮮食材，傳遞出家常卻不平凡的溫度。 印月餐廳｜中式料理的藝術演繹，宴客與家庭聚會首選
說到臺中公益路的中式料理代表，印月餐廳 絕對是榜上有名。這間開業多年的餐廳以「中菜西吃」的概念聞名，把傳統中式料理以現代手法重新詮釋。從建築外觀到餐具擺設，每個細節都散發著低調的典雅氣息。 餐點特色
印月最令人印象深刻的是他們將傳統中菜融入創意手法。 用餐體驗服務方面完全對得起餐廳的高級定位。從入座、點餐到上菜節奏，都拿捏得恰如其分。每道菜都會有服務人員細心介紹食材與吃法，讓人感受到「被款待」的尊榮感。 綜合評分
地址：408臺中市南屯區公益路二段818號電話：0422511155 小結語印月餐廳是一間「不只吃飯，更像品味生活」的地方。 KoDō 和牛燒肉｜極致職人精神，專為儀式感與頂級味覺而生
若要形容 KoDō 和牛燒肉 的用餐體驗，一句話足以總結——「像在欣賞一場關於肉的表演」。 餐點特色
這裡主打 日本A5和牛冷藏肉，以「精切厚燒」的方式呈現。 用餐體驗KoDō 的最大特色是「儀式感」。 綜合評分
地址：403臺中市西區公益路260號電話：0423220312 官網：https://www.facebook.com/kodo2018/ 小結語KoDō 和牛燒肉不是日常餐廳，而是一場體驗。 永心鳳茶｜在茶香裡用餐的優雅時光，臺味早午餐的新詮釋
走進 永心鳳茶公益店，彷彿進入一間有氣質的茶館。 餐點特色
永心鳳茶的餐點結合中式靈魂與西式擺盤，無論是「炸雞腿飯」還是「紅玉紅茶拿鐵」，都能讓人感受到熟悉卻不平凡的味道。 用餐體驗店內服務人員態度溫和，對茶品介紹詳盡。上餐節奏剛好，不急不徐。 綜合評分
地址：40360臺中市西區公益路68號三樓(勤美誠品)電話：0423221118 小結語永心鳳茶讓人重新定義「臺味」。 三希樓｜老饕級江浙功夫菜，穩重又帶人情味的中式饗宴
位於公益路上的 三希樓 是許多臺中老饕的口袋名單。 餐點特色
三希樓的菜色以 江浙與港式料理 為主，兼顧傳統與現代風味。 用餐體驗三希樓的服務給人一種老派但貼心的感覺。 綜合評分
地址：408臺中市南屯區公益路二段95號電話：0423202322 官網：https://www.sanxilou.com.tw/ 小結語三希樓是一間「吃得出功夫」的餐廳。 一笈壽司｜低調奢華的無菜單日料，職人手藝詮釋旬味極致
在熱鬧的公益路上，一笈壽司 低調得幾乎不顯眼。 餐點特色
一笈壽司採 Omakase（無菜單料理） 形式，每一餐都由主廚根據當日食材設計。 用餐體驗整場用餐約90分鐘，節奏緩慢但沉穩。 綜合評分
地址：408臺中市南屯區公益路二段25號電話：0423206368 官網：https://www.facebook.com/YIJI.sushi/ 小結語一笈壽司是一間真正讓人「放慢呼吸」的餐廳。 茶六燒肉堂｜人氣爆棚的和牛燒肉聖地，肉香與幸福感同時滿分
若要票選公益路上「最難訂位」的餐廳，茶六燒肉堂 絕對名列前茅。 餐點特色
茶六主打 和牛燒肉套餐，價格約落在 $700–$1000 間，份量與品質兼具。 用餐體驗茶六的服務效率相當高。店員親切、換網勤快、補水速度快，整場用餐流程流暢無壓力。 綜合評分
地址：403臺中市西區公益路268號電話：0423281167 官網：https://inline.app/booking/-L93VSXuz8o86ahWDRg0:inline-live-karuizawa/-LUYUEIOYwa7GCUpAFWA 小結語茶六燒肉堂用「穩定品質＋輕奢氛圍」抓住了臺中年輕族群的心。 吃完10家公益路餐廳後的心得與結語吃完這十家餐廳後，臺中公益路不只是一條美食街，而是一段生活風景線。 有的餐廳講究細膩與儀式感，像 一頭牛日式燒肉 與 一笈壽司，讓人感受到食材最純粹的美好 有的則以親切與溫度打動人心，像 加分昆布鍋物、永心鳳茶，讓人明白吃飯不只是為了飽足，而是一種被照顧的幸福。 而像茶六燒肉堂、TANG Zhan 湯棧 這類人氣名店，則用穩定的品質與熱絡的氛圍，成為許多臺中人心中「想吃肉就去那裡」的代名詞。 這十家店，構成了公益路最動人的縮影 有華麗的，也有溫柔的；有傳統的，也有創新的。 每一家都在自己的風格裡發光，讓人吃到的不只是料理，而是一種生活的溫度與節奏。 對我而言，這不僅是一場美食旅程，更是一趟關於「臺中味道」的回憶之旅。 FAQ：關於臺中公益路美食常見問題Q1：公益路哪一區的餐廳最集中？ Q2：需要提前訂位嗎？ 最後的話若要用一句話形容這趟美食之旅，我會說： 永心鳳茶小孩適合去嗎？ 如果你也和我一樣喜歡用味蕾探索一座城市，那就把這篇公益路美食攻略收藏起來吧。印月餐廳適合請客嗎？ 無論是約會、慶生、家庭聚餐，或只是想犒賞一下辛苦的自己——這條路上永遠會有一間剛剛好的餐廳在等你。一頭牛日式燒肉尾牙預算好掌控嗎？ 下一餐，不妨從這10家開始。永心鳳茶份量足夠嗎？ 打開手機、約上朋友，讓公益路成為你生活裡最容易抵達的小確幸。三希樓清淡口味適合嗎？ 如果你有私心愛店，也歡迎留言分享，一頭牛日式燒肉婚前派對適合嗎？ 你的推薦，可能讓我下一趟美食旅程變得更精彩。三希樓需要訂位嗎？ Researchers have conducted a comprehensive study on how serotonin affects behavior using the nematode worm C. elegans. They found that the worm’s six serotonin receptors each play distinct roles, with three driving behavioral slowing and the rest modulating their function. The study provides insight into the complexities of the serotonergic system and implications for psychiatric drug development. Scientists at The Picower Institute for Learning and Memory at MIT have provided comprehensive insight into how serotonin affects behavior in a study using the nematode worm C. elegans, a simple animal model. The research team identified the functional roles of the worm’s six serotonin receptors by creating 64 different mutant strains, each missing different combinations of receptors. They discovered that three receptors primarily drove the slowing behavior associated with serotonin release, while the other three receptors interacted with the primary receptors and modulated their function. Furthermore, different receptors were found to respond to different patterns of serotonin release. By fluorescently tagging each receptor gene in each neuron across the brain, the team observed how serotonin’s effects worked at a circuit level. The study provides a view of the complexities and opportunities for the development of psychiatric drugs that target the serotonergic system. Because serotonin is one of the primary chemicals the brain uses to influence mood and behavior, it is also the most common target of psychiatric drugs. To improve those drugs and to invent better ones, scientists need to know much more about how the molecule affects brain cells and circuits both in health and amid disease. In a new study, researchers at The Picower Institute for Learning and Memory at MIT working in a simple animal model present a comprehensive accounting of how serotonin affects behavior from the scale of individual molecules all the way to the animal’s whole brain. “There have been major challenges in rationally developing psychiatric drugs that target the serotonergic system,” said Steve Flavell, associate professor in The Picower Institute and MIT’s Department of Brain and Cognitive Sciences, and senior author of the study in Cell. “The system is wildly complex. There are many different types of serotonergic neurons with widespread projections throughout the brain and serotonin acts through many different receptors, which are often activated in concert to change the way that neural circuits work.” A 3D rendering of a C. elegans worm, mapping all of its neurons. Credit: Steve Flavell/MIT Picower Institute These same complexities that scientists face in people are all afoot in the nematode worm C. elegans, but to a more manageably limited degree. C. elegans has only 302 neurons (rather than billions) and only six serotonin receptors (rather than the 14 found in people). Moreover, all C. elegans neurons and their connections have been mapped out and its cells are accessible for genetic manipulation. Finally, Flavell’s team has developed imaging technologies that enable them to track and map neural activity across the worm’s brain simultaneously. For all these reasons, the lab was able to produce a novel study revealing how the far-reaching molecular activity of serotonin changes brain-wide activity and behavior. “These results provide a global view of how serotonin acts on a diverse set of receptors distributed across a connectome to modulate brain-wide activity and behavior,” the research team wrote in Cell. The study’s co-lead authors are Picower Institute postdoc Ugur Dag, MIT Brain and Cognitive Sciences graduate student Di Kang, and former research technician Ijeoma Nwabudike, who is now a MD-PhD student at Yale. Slowing for Savoring Flavell showed in Cell in 2013 that C. elegans uses serotonin to slow down when it reaches a patch of food and traced its source to a neuron called NSM. In the new study, the team used their many new capabilities developed since then at MIT to examine serotonin’s effects comprehensively. First, they focused on identifying the functional roles of the worm’s six serotonin receptors. To do that they created 64 different mutant strains covering the different combinations of knocking out the various receptors. For instance, one strain would have just one receptor knocked out while another strain would have all but that one missing and another would be missing three. In each of these worms the team stimulated serotonin release from the NSM neuron to prompt slowing behaviors. Analysis of all the resulting data revealed at least two key findings: One was that three receptors primarily drove the slowing behavior. The second was that the other three receptors “interacted” with the receptors that drive slowing and modulated how they function. These complex interactions between serotonin receptors in the control of behavior is likely to be directly relevant to psychiatric drugs that target these receptors, Flavell said. A wiring diagram of the C. elegans worm shows neurons and muscle cells (dots) that express receptors for serotonin. Each color denotes a specific receptor. Some neurons express more than one. The diagram appears as a figure in the research paper. Credit: Di Kang/MIT Picower Institute The researchers also gained other important insights into serotonin’s actions. One was that different receptors respond to different patterns of serotonin release in live animals. For example, the SER-4 receptor only responded to sudden increases in serotonin release by the NSM neuron. However, the MOD-1 receptor responded to continuous “tonic” changes in serotonin release by NSM. This suggests that different serotonin receptors are engaged at different times in the live animal. Brain-Wide Mapping Having teased out the roles of the serotonin receptors in the control of C. elegans behavior, the research team then used their imaging technologies to see how serotonin’s effects worked at a circuit level. For instance, they fluorescently tagged each receptor gene in each neuron across the brain so that they could see all the specific cells that expressed each receptor, providing a brain-wide map of where the serotonin receptors are located in C. elegans. About half of the worm’s neurons express serotonin receptors with some neurons expressing as many as five different types. Finally, the team used their ability to track all neuron activity (based on their calcium fluctuations) and all behaviors to watch how the serotonergic neuron NSM affected other cells’ activity as worms freely explored their surroundings. About half of the neurons across the worm’s brain changed activity when serotonin was released. Since they knew which exact neurons they were recording from, the research team asked whether knowing which serotonin receptors each cell expressed could predict how they responded to serotonin. Indeed, knowing which receptors were expressed in each neuron and its input neurons gave strong predictive power of how each neuron was impacted by serotonin. “We performed brain-wide calcium imaging in freely-moving animals with knowledge of cellular identity during serotonin release, providing, for the first time, a view of how serotonin release is associated with changes in activity across the defined cell types of an animal’s brain,” the researchers concluded. All these findings shed light on the kinds of complexities and opportunities facing drug developers, Flavell noted. The study’s findings show how the effects of targeting one serotonin receptor could depend on how other receptors or the cell types that express them are functioning. In particular, the study highlights how the serotonin receptors act in concert to change the activity states of neural circuits. Reference: “Dissecting the functional organization of the C. elegans serotonergic system at whole-brain scale” by Ugur Dag, Ijeoma Nwabudike, Di Kang, Matthew A. Gomes, Jungsoo Kim, Adam A. Atanas, Eric Bueno, Cassi Estrem, Sarah Pugliese, Ziyu Wang, Emma Towlson and Steven W. Flavell, 15 May 2023, Cell. DOI: 10.1016/j.cell.2023.04.023 In addition to Flavell, Dag, Nwabudike and Kang, the paper’s other authors are Matthew Gomes, Jungsoo Kim, Adam Atanas, Eric Bueno, Cassi Estrem, Sarah Pugliese, Ziyu Wang and Emma Towlson. Study funders included the National Institutes of Health, the National Science Foundation, the McKnight Foundation, the Alfred P. Sloan Foundation, the Picower Institute and the JPB Foundation. When a cytokine (green) binds to receptors (teal), two parts of the Janus kinase protein (pink) come together, activating it to send signals inside a cell. In some cancers, mutations in the kinase lock it together, keeping it abnormally active. Credit: Eric Smith/Chris Garcia/Howard Hughes Medical Institute Stanford researchers have captured the 3D structure of a crucial signaling protein, Janus kinase, revealing how it functions and malfunctions in diseases like cancer. This breakthrough could lead to more precise drug development. The breakthrough came on molecular biologist Christopher Garcia’s birthday. For more than 20 years, his team and others around the world had been chasing an elusive quarry – the 3D structure of a crucial signaling protein in cells. In late 2021, his electron microscope images of the molecule started to come into focus. On December 8, postdoc Naotaka Tsutsumi and graduate student Caleb Glassman sent him an email with a startlingly clear picture of the protein latched on to a key receptor. “I was sitting in a meeting, and I realized we had it,” recalls Garcia, a Howard Hughes Medical Institute Investigator at Stanford University. “I immediately left the meeting and ran back to the lab.” Glassman, who had just moved to Boston for a Harvard postdoc, canceled his planned backcountry trip, and rushed back to Stanford. “I wanted to finish what Naotaka and I had started,” he explains. Then the three researchers worked around the clock to nail the complete structure of the protein, known as a Janus kinase, and beat competing labs to the discovery. “It was a big horse race between many great groups worldwide, and we were sprinting towards the finish line,” Garcia says. On December 26, they rushed a manuscript to the journal Science, which published the work on March 10, 2022. Garcia’s team has nabbed not just the full structure of a vitally important signaling molecule, but also the mechanism for how these kinases work, which had been “a fundamental question in biology,” says John O’Shea, an immunologist at the National Institutes of Health who helped to develop one of the first drugs to block Janus kinase function and was not involved with the new research. Because the proteins can go awry in disease, the results could lead to new and better drugs against certain cancers. “It’s amazing work,” O’Shea says. Chipping Away Janus kinases are one of the communication whizzes of the animal kingdom. They take signals that come from outside cells and pass the info along to molecules inside. Scientists have known for years that malfunctioning Janus kinases can cause disease. Some mutations that impair Janus kinases can severely curtail the body’s ability to fight off infection, causing a condition virtually identical to “bubble boy disease.” And when genetic glitches and exaggerated signals rev up the kinases too much, the result can be blood cancers like leukemia, and allergic or autoimmune diseases. Researchers knew the shape of parts of the proteins, including related enzyme and regulatory regions at the end of the molecule, which earned them the name Janus kinases, after the two-faced mythological Roman god. And sophisticated drug screens have unearthed molecules that inhibit these proteins, giving doctors a way to treat some cancers and disorders like rheumatoid arthritis. But scientists developed the drugs without knowing the molecules’ full structure or how they become activated. So most of the current arsenal of nearly a dozen drugs, plus more in clinical trials, are relatively blunt instruments, blocking both healthy and mutated Janus kinases. They can still treat many diseases, from eczema to COVID-19, but also can cause a range of side effects. Garcia wanted a more detailed view of the proteins but, as he learned when he first tried to image the molecules as a postdoc in 1995, it was a daunting challenge. The kinases are notoriously difficult to make in the lab. And they don’t easily form crystals, which scientists need to capture 3D structures using x-ray crystallography. So, for many years, Garcia and others could only view bits of the kinases at a time. “We kept chipping away without much to show for it,” he says. In the last few years, the pieces began to fall into place. One key advance was a method called cryo-EM, where scientists freeze samples and then view them using an electron microscope. Another was the choice by Garcia’s team to study a mouse Janus kinase rather than a less stable human one. They also introduced a common cancer-causing mutation into the mouse kinase, which stabilized the molecule even further. Lighting a Fire Garcia’s team’s work reveals the structure of a Janus kinase called JAK1 and outlines the steps it uses to sends signals within cells. First, receptor proteins stud cell membranes, poking from the inner and outer surfaces of the cell like a toothpick through a sandwich. Then, a single Janus kinase inside the cell attaches to the receptors, waiting for a signal. Next, molecules called cytokines approach the cell’s exterior, each binding to two receptors. The cytokines act like a bridge that pulls the two receptors even closer, Garcia explains. That brings the active ends of the Janus kinase together, switching them on. Like a match lighting a fire, the kinase relays a signal that tells genes to turn on or off. The structure also reveals how the cancer-causing mutation short-circuits this messaging chain – by gluing two parts of the Janus kinase together. That causes the two active regions to stay switched on even when there are no outside cytokines, sparking uncontrolled activity that can trigger cancers. Garcia hopes the new results could help scientists design better drugs that target only defective Janus kinases, allowing healthy versions to keep performing their normal duties. The work, he says, is an example of an “ideal situation in science, where solving a basic problem also has direct relevance for disease.” Reference: “Structure of a Janus kinase cytokine receptor complex reveals the basis for dimeric activation” by Caleb R. Glassman, Naotaka Tsutsumi, Robert A. Saxton, Patrick J. Lupardus, Kevin M. Jude and K. Christopher Garcia, 10 March 2022, Science. DOI: 10.1126/science.abn8933 Origin of life artist’s conception. Experiment sheds light on the molecular evolution of RNA. Researchers at the University of Tokyo have for the first time been able to create an RNA molecule that replicates, diversifies, and develops complexity, following Darwinian evolution. This has provided the first empirical evidence that simple biological molecules can lead to the emergence of complex lifelike systems. “Honestly, we initially doubted that such diverse RNAs could evolve and coexist.” Ryo Mizuuchi Life has many big questions, not least being where did we come from? Maybe you’ve seen the T-shirts with pictures going from ape to human (to tired office worker). But how about from simple molecule to complex cell to ape? For several decades, one hypothesis has been that RNA molecules (which are vital for cell functions) existed on primitive Earth, possibly with proteins and other biological molecules. Then around 4 billion years ago, they started to self-replicate and develop from a simple single molecule into diverse complex molecules. This step-by-step change possibly eventually led to the emergence of life as we know it — a beautiful array of animals, plants, and everything in between. Although there have been many discussions about this theory, it has been difficult to physically create such RNA replication systems. However, in a study published in Nature Communications, Project Assistant Professor Ryo Mizuuchi and Professor Norikazu Ichihashi at the Graduate School of Arts and Sciences at the University of Tokyo, and their team, explain how they carried out a long-term RNA replication experiment in which they witnessed the transition from a chemical system towards biological complexity. RNA molecules were incubated in water-in-oil droplets at 37 degrees Celsius for 5 hours. The solution was then diluted to one-fifth the concentration using new droplets containing RNA-free nutrients, and stirred vigorously. When this process was repeated multiple times, mutations occurred. Credit: © modified from Mizuuchi 2022 The Darwinian Evolution of RNA Molecules The team was truly excited by what it saw. “We found that the single RNA species evolved into a complex replication system: a replicator network comprising five types of RNAs with diverse interactions, supporting the plausibility of a long-envisioned evolutionary transition scenario,” said Mizuuchi. Compared to previous empirical studies, this new result is novel because the team used a unique RNA replication system that can undergo Darwinian evolution, i.e., a self-perpetuating process of continuous change based on mutations and natural selection, which enabled different characteristics to emerge, and the ones that were adapted to the environment to survive. “Honestly, we initially doubted that such diverse RNAs could evolve and coexist,” commented Mizuuchi. “In evolutionary biology, the ‘competitive exclusion principle’ states that more than one species cannot coexist if they are competing for the same resources. This means that the molecules must establish a way to use different resources one after another for sustained diversification. They are just molecules, so we wondered if it were possible for nonliving chemical species to spontaneously develop such innovation.” Future Directions in Understanding Life’s Origins So what next? According to Mizuuchi, “The simplicity of our molecular replication system, compared with biological organisms, allows us to examine evolutionary phenomena with unprecedented resolution. The evolution of complexity seen in our experiment is just the beginning. Many more events should occur towards the emergence of living systems.” Of course, there are still many questions left to answer, but this research has provided further empirically based insight into a possible evolutionary route that an early RNA replicator may have taken on primitive Earth. As Mizuuchi said, “The results could be a clue to solving the ultimate question that human beings have been asking for thousands of years — what are the origins of life?” Reference: “Evolutionary transition from a single RNA replicator to a multiple replicator network” by Ryo Mizuuchi, Taro Furubayashi and Norikazu Ichihashi, 18 March 2022, Nature Communications. DOI: 10.1038/s41467-022-29113-x This research is mainly supported by Grant-in-Aid for Scientific Research (Assignment No.: JP19K23763, JP21H05867, JP15KT0080, JP18H04820, JP20H04859), JST PRESTO (Assignment No.: JPMJPR19KA), Astrobiology Center Project Research (Assignment No. AB021005). RRG455KLJIEVEWWF |
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