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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: 一頭牛日式燒肉情侶來合適嗎? 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。KoDō 和牛燒肉慶生氛圍夠嗎? 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。KoDō 和牛燒肉春酒菜色豐富嗎? 下一餐,不妨從這10家開始。一笈壽司單點比較好嗎? 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。TANG Zhan 湯棧停車方便嗎? 如果你有私心愛店,也歡迎留言分享,永心鳳茶停車方便嗎? 你的推薦,可能讓我下一趟美食旅程變得更精彩。永心鳳茶價位會不會太高? Artistic representation of numerical discrimination in Drosophila. Credit: Mercedes Bengochea, Maria Ines Oviedo In a study at the Paris Brain Institute, fruit flies demonstrated numerical sensitivity, preferring larger quantities and distinguishing between quantities based on clear ratios. The crucial role of LC11 neurons in this skill was identified, highlighting the cognitive capabilities of insects and their importance in understanding human brain function. In the animal world, you don’t need to learn a numeral system – such as the ten-digit Indo-Arabic system we commonly use – to be able to count. Animals constantly use numerical information from their environment to make decisions. Estimating the number of conspecifics in a competing group before engaging in conflict, the amount of food available in a difficult-to-reach location, or the number of potential sexual partners in a new territory is essential for survival and reproduction. This skill can reach an astonishing level of refinement; for example, certain species of ants orient themselves in the desert by estimating the number of steps required to reach a target. Animals’ Numerical Sensitivity and Neural Correlates “Numerical sensitivity, i.e., the ability to perceive information related to quantities, exists in many vertebrates and invertebrates. It has been documented in primates, birds, amphibians, fish, and bees, explains Mercedes Bengochea, a post-doctoral researcher in Bassem Hassan’s team at Paris Brain Institute. You don’t need to enumerate numbers to distinguish between one, two, several and many! However, we didn’t know which neuronal circuits were involved in this skill.” To investigate this question, researchers must record the brain activity of an animal during a numerical task, then activate or deactivate specific neural cells to determine which areas of the brain are involved. These operations are difficult to carry out on vertebrates, but the right tools already exist with fruit flies. “Drosophila melanogaster is a model of choice for studying cognition. These insects adjust their behavior in the face of a threat according to the number of fellow flies who could help, adds the researcher. In the event of imminent danger, the smaller the size of its group, the more likely they are to freeze to stay safe.” Fruit Flies’ Numeric Perception: An Exploration To determine whether fruit flies can accurately evaluate numbers and assign values to perceived quantities, Mercedes Bengochea and her colleagues used an experimental setting that has already proven its relevance. They placed the flies in arenas called “Buridan arenas,” where they were exposed to visual stimuli: in that case, two sets of objects. The researchers then determined which stimulus the insects preferred by measuring the time they spent inspecting either set. Their results indicate that fruit flies stayed longer near the set containing three objects than the set that had only one – regardless of the size of the objects or the total volume occupied by the set. This taste for larger quantities was preserved when the insects had to choose between groups of 2 or 4 objects and 2 or 3 objects. “The flies, however, were unable to distinguish between sets of respectively 3 and 4 objects, explains Mercedes Bengochea. It seems that the ratio between these two numbers is not sufficient for them to perceive a difference. On the other hand, they can very easily compare a group of 4 and a group of 8 objects – a ratio of simple to double”. Fruit flies are, therefore, not limited to counting to 3: the ratio between the quantities evaluated must be clear enough to be perceived. Assessing Ratios: A Common Animal Skill Comparing two quantities is a simple visual task common in many animals, including humans. It helps us estimate the size of a large group at a glance, such as a crowd at a concert that contains too many people to be counted one by one. Identifying the Neural Circuits Involved Which neural circuits are involved in this system of numerical discrimination in Drosophila remains to be determined. To do this, the researchers successively “switched off” different areas of the insects’ brains, preventing the transmission of nerve signals at synapses. After several tests, they observed that the activity of a column of neurons located in the optic lobe, LC11 neurons (for lobular columnar neurons 11), was necessary for flies to distinguish different sets of objects. “In a second experiment, we taught the insects to go against their natural inclination for large numbers, using a simple conditioning method: an appetizing dose of sugar was placed next to the smallest sets of objects, adds the researcher. Momentarily, thanks to the lure of the food, we made them prefer the small numbers. But once the LC11s had been inactivated, the insects no longer showed any preference… for either large or small quantities. This confirms that these neurons are essential for comparing quantities, regardless of the value fruit flies assign to them.” LC11s are also involved in the social behavior of fruit flies: they are activated when insects must adapt their defense strategy according to the number of congeners flying nearby. “We believe that the ability to assess quantities has been decisive in the evolution of invertebrates, explains Bassem Hassan, head of the ‘Brain Development’ team. The cognitive solutions insects use to ‘count’ are very simple. Several studies have shown that, in a computational model, a few artificial neurons are enough to perform a numerical task.” Flies will never help us do our accounting. However, like other insects, we are often tempted to underestimate their cognitive abilities and the subtlety of their social behavior. It’s a mistake made even more regrettable because, without them, our understanding of the human brain would remain terribly limited. Reference: “Numerical discrimination in Drosophila melanogaster” by Mercedes Bengochea, Jacobo D. Sitt, Veronique Izard, Thomas Preat, Laurent Cohen and Bassem A. Hassan, 14 July 2023, Cell Reports. DOI: 10.1016/j.celrep.2023.112772 Researchers from UNC School of Medicine are using evolutionary genomics to understand human diseases. They focus on unchanged, highly constrained genes through the mammalian evolution. This new perspective allows tracing of psychiatric and neurological disorders to alterations in these genes. This could provide insights into various mental health conditions and possibly allow researchers to lessen the effects of genetic diseases by manipulating certain DNA sequences. A team of scientists has created a new manual researchers can use to learn more about the origins of human diseases with high genetic risk. Hundreds of scientific studies have been conducted over the years to find the genes underlying common human traits, from eye color to intelligence and physical and mental illnesses. Patrick Sullivan, MD, FRANZCP, the Yeargan Distinguished Professor of Psychiatry and Genetics at the University of North Carolina (UNC) School of Medicine, and the Psychiatric Genomic Consortium have produced a new packet for the journal Science, to give researchers another way to understand human disease, using the power of evolutionary genomics. “This is a tool that can give us a lot of important hints about human disease,” said Sullivan, who is also a professor at the Karolinska Institute in Stockholm, Sweden. “If we can take a deep dive into your genome, we can get some idea about your ancestors, both human and nonhuman, and observe the impacts of many millions of years of evolution in you.” Most cells of the body have 46 chromosomes, grouped into 23 pairs. Each chromosome is made up of a string of deoxyribonucleic acid (DNA), the genetic material that provides instructions for how the body grows and functions. Credit: Psychiatric Genomics Consortium What Makes Us Mammals Every single living organism on the planet has DNA. The self-replicating material acts as a blueprint for producing certain molecules in organisms, such as proteins. It’s no surprise that humans and our closest relatives, chimpanzees, share 98.8% of genetic material. While some of our genes have evolved over time, others have remained the same throughout the entire mammalian evolutionary process. In scientific terms, these are called “highly constrained” genes. Some human genes have a surprising amount of genetic similarity in mice, cows, dogs, cats, bats, and dolphins in many regions of the genome. These are the genes that unite us as mammals. Since these genes have undergone a “trial by fire” throughout evolutionary history, these unaltered genetic regions must play a fundamental role in the health and genetic makeup of the organism, according to Sullivan. Patrick Sullivan, MD, FRANZCP. Credit: UNC Department of Psychiatry “Some highly constrained genes can make proteins that are nearly identical in us and in a mouse,” said Sullivan. “That’s crazy because we have probably 60 million years of evolution between us and the mouse. And yet, this protein hasn’t changed so we infer that this protein is doing something really important.” It might be simpler to see the work of our shared genes when we zoom out to take a more holistic view. Humans and other mammals share anatomical structures, such as the four-chambered heart, lungs, hair (or fur), skeleton, and milk-producing mammary glands. We also share similar fundamental processes on a smaller scale, including embryology, how cells grow and divide, and the development and operation of the synapses that transmit neurological chemicals throughout our bodies and brains. All of which are formed through our shared genetic regions. So, if one of these genes that make up the basics of a mammal is altered or deleted, it could have negative effects on the organism. A New Way to Look at Human Mental and Physical Health If a patient has a neurological brain disorder or certain psychiatric disorders, researchers are able to trace it back and see that this person has received a “big hit” to one of the highly constrained genes that are critical to the nervous system, brain structure, or synapses. Many researchers have relied on the genome-wide association study (GWAS) to find where the genetic risk for a disease is located in the genome. Using genomic techniques and large-size samples, researchers can analyze the entire genome of many populations to find genetic variations, such as single nucleotide polymorphisms (SNPs), associated with a disease or a trait. Even though it is important to know where these variations are located in the genome, it’s also useful to know how or why these genetic variations happened in the first place. Sullivan hopes that other researchers will make use of the new and extensive document to reach their own conclusions regarding the genetics underlying a variety of human diseases. “As it turns out, a lot of brain traits are actually highly conserved,” said Sullivan, who serves as director of the UNC Suicide Prevention Institute in the Department of Psychiatry. “This research project has really given me a much, much deeper understanding of the genome and how the genome is set up. I now use this all the time in trying to understand schizophrenia, suicide, depression, and eating disorders.” What This Means for Future Research As one can imagine, the successful development of a human requires heavy lifting from proteins and DNA sequences. There are two short regions within our DNA, called regulatory enhancers and regulatory promoters, which play especially important roles in regulating our DNA. The creation of a human gene is similar to a factory that produces donuts. Regulatory enhancers are responsible for controlling the amount of dough squeezed out of the machine and onto the baking tray. Promoters, on the other hand, are in control of when the dough is being squirted onto the tray. At the end of the day, you have a full formed gene. Researchers like Sullivan may be able to go into the DNA sequences and increase or decrease these regulatory enhancers and promoters to affect the amount of proteins produced by genes, with the goal of lessening the effects of a genetically based disease. “It might be possible to hit the upstream part that controls it, in a very soft way, to see if that actually helps,” says Sullivan. Reference: “Leveraging base-pair mammalian constraint to understand genetic variation and human disease” by Patrick F. Sullivan, Jennifer R. S. Meadows, Steven Gazal, BaDoi N. Phan, Xue Li, Diane P. Genereux, Michael X. Dong, Matteo Bianchi, Gregory Andrews, Sharadha Sakthikumar, Jessika Nordin, Ananya Roy, Matthew J. Christmas, Voichita D. Marinescu, Chao Wang, Ola Wallerman, James Xue, Shuyang Yao, Quan Sun, Jin Szatkiewicz, Jia Wen, Laura M. Huckins, Alyssa Lawler, Kathleen C. Keough, Zhili Zheng, Jian Zeng, Naomi R. Wray, Yun Li, Jessica Johnson, Jiawen Chen, Zoonomia Consortium§. , Benedict Paten, Steven K. Reilly, Graham M. Hughes, Zhiping Weng, Katherine S. Pollard, Andreas R. Pfenning, Karin Forsberg-Nilsson, Elinor K. Karlsson, Kerstin Lindblad-Toh, Gregory Andrews, Joel C. Armstrong, Matteo Bianchi, Bruce W. Birren, Kevin R. Bredemeyer, Ana M. Breit, Matthew J. Christmas, Hiram Clawson, Joana Damas, Federica Di Palma, Mark Diekhans, Michael X. Dong, Eduardo Eizirik, Kaili Fan, Cornelia Fanter, Nicole M. Foley, Karin Forsberg-Nilsson, Carlos J. Garcia, John Gatesy, Steven Gazal, Diane P. Genereux, Linda Goodman, Jenna Grimshaw, Michaela K. Halsey, Andrew J. Harris, Glenn Hickey, Michael Hiller, Allyson G. Hindle, Robert M. Hubley, Graham M. Hughes, Jeremy Johnson, David Juan, Irene M. Kaplow, Elinor K. Karlsson, Kathleen C. Keough, Bogdan Kirilenko, Klaus-Peter Koepfli, Jennifer M. Korstian, Amanda Kowalczyk, Sergey V. Kozyrev, Alyssa J. Lawler, Colleen Lawless, Thomas Lehmann, Danielle L. Levesque, Harris A. Lewin, Xue Li, Abigail Lind, Kerstin Lindblad-Toh, Ava Mackay-Smith, Voichita D. Marinescu, Tomas Marques-Bonet, Victor C. Mason, Jennifer R. S. Meadows, Wynn K. Meyer, Jill E. Moore, Lucas R. Moreira, Diana D. Moreno-Santillan, Kathleen M. Morrill, Gerard Muntané, William J. Murphy, Arcadi Navarro, Martin Nweeia, Sylvia Ortmann, Austin Osmanski, Benedict Paten, Nicole S. Paulat, Andreas R. Pfenning, BaDoi N. Phan, Katherine S. Pollard, Henry E. Pratt, David A. Ray, Steven K. Reilly, Jeb R. Rosen, Irina Ruf, Louise Ryan, Oliver A. Ryder, Pardis C. Sabeti, Daniel E. Schäffer, Aitor Serres, Beth Shapiro, Arian F. A. Smit, Mark Springer, Chaitanya Srinivasan, Cynthia Steiner, Jessica M. Storer, Kevin A. M. Sullivan, Patrick F. Sullivan, Elisabeth Sundström, Megan A. Supple, Ross Swofford, Joy-El Talbot, Emma Teeling, Jason Turner-Maier, Alejandro Valenzuela, Franziska Wagner, Ola Wallerman, Chao Wang, Juehan Wang, Zhiping Weng, Aryn P. Wilder, Morgan E. Wirthlin, James R. Xue and Xiaomeng Zhang, 28 April 2023, Science. DOI: 10.1126/science.abn2937 Composite of an embryonic mouse eye cup (E14.5) labeled with antibodies against the developmental transcription factors Lhx2 (red) and Otx2 (green), and cultured human retinal pigmented epithelium (RPE) labeled with antibodies against MITF (red) and ZO-1 (green). Credit: Images by Mazal Cohen-Gulkar, composite by Ruth Ashery-Padan (CC-BY 4.0) Researchers Have Uncovered New Insights Into the Causes of Adult-Onset Macular Degeneration A new study by Ran Elkon and Ruth Ashery-Padan of Tel Aviv University and colleagues has revealed a previously unknown genetic risk factor for adult-onset macular degeneration (AMD) by combining a map of gene regulatory sites with disease-related loci. This discovery advances the knowledge of the main cause of visual loss in adults. The findings were recently published in the journal PLOS Biology. The leading cause of adult-onset macular degeneration (AMD) is due to a breakdown in the function of the retinal pigmented epithelium (RPE), a layer of tissue between the photoreceptors that detect light and the choriocapillaris that provides nourishment to the retina. Recognizing the significance of RPE in the development of AMD, the authors of the study focused on exploring the role of a transcription factor called LHX2. The team’s analysis of mouse mutants showed that LHX2 plays a crucial role in RPE development. LHX2: A Key Transcription Factor in RPE Development Knocking down LHX2 activity in RPE derived from human stem cells, they found that most affected genes were down-regulated, indicating that LHX2’s role was likely that of a transcriptional activator, binding to regulatory sites on the genome to increase the activity of other genes. The authors found that one affected gene, called OTX2, collaborated with LHX2 to regulate many genes in the RPE. By mapping the genomic sites that OTX2 and LHX2 could bind to, they showed that 68% of those that bound LHX2 were also bound by OTX2 (864 sites in all), suggesting they likely work together to promote the activity of a large suite of genes involved in RPE development and function. A common method for finding genes that may contribute to a disease is to perform a genome-wide association study (GWAS), which identifies genome sequence differences between individuals (termed single nucleotide polymorphisms, or SNPs) that co-occur with the disease. Numerous such studies have previously been done in AMD. However, a GWAS by itself cannot uncover a causal mechanism. Here, the authors compared their LHX2/OTX2 binding data to GWAS data in order to home in on variations that affected the binding of the transcription factors, and thus may contribute to disease. Linking TRPM1 to AMD Risk via LHX2 Binding One such binding site was located within the promoter region of a gene called TRPM1, which had been previously linked to AMD, and found that the sequence variant at that site altered the binding strength of LHX2; the so-called C version bound it more strongly than the T version, and activity of the TRPM1 gene was higher when the C allele was present instead of the T allele. The results of the study indicate that the previously known increased risk of AMD from the variant identified in the GWAS was due to a reduction in the binding of the LHX2 transcription factor to the TRPM1 gene promoter, with a consequent reduction in the activity of this gene. The gene encodes a membrane ion channel, and previous studies have shown that mutations in the gene also cause visual impairment. “Our study exemplifies how delineation of tissue-specific transcriptional regulators, their binding sites across the genome, and their downstream gene-regulatory networks can provide insights into a complex disease’s pathology,” the authors said. Ashery-Padan adds, “The findings reveal a regulatory module consisting of LHX2 and OTX2 that controls the development and maintenance of the retinal pigmented epithelium, an important tissue of visual function. The genomic analyses further link the genomic regions bound by the two developmental factors to the genetics of the common, multifactorial blinding disease age-related macular degeneration (AMD).” Reference: “The LHX2-OTX2 transcriptional regulatory module controls retinal pigmented epithelium differentiation and underlies genetic risk for age-related macular degeneration” by Mazal Cohen-Gulkar, Ahuvit David, Naama Messika-Gold, Mai Eshel, Shai Ovadia, Nitay Zuk-Bar, Maria Idelson, Yamit Cohen-Tayar, Benjamin Reubinoff, Tamar Ziv, Meir Shamay, Ran Elkon and Ruth Ashery-Padan, 17 January 2023, PLOS Biology. DOI: 10.1371/journal.pbio.3001924 RRG455KLJIEVEWWF |
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