VOA文化艺术2025 科学家将基因与人类语言联系起来(在线收听) |
科学家将基因与人类语言联系起来 Scientists Link Gene to Human Speech The research identifies a protein – found only in people – that may have helped early humans develop spoken communication. 这项研究发现了一种只存在于人类体内的蛋白质,这种蛋白质可能有助于早期人类发展口语交流。 Scientists involved in the study say this new speaking ability became important for humans' survival. 参与这项研究的科学家表示,这种新的说话能力对人类的生存至关重要。 For example, speech permitted individuals to share information, organize activities and pass down knowledge. 例如,言语允许个人分享信息、组织活动和传递知识。 These abilities are now seen as an advantage humans had over their relatives, such as the Neanderthals and Denisovans. 这些能力现在被认为是人类比他们的亲戚,如尼安德特人和丹尼索瓦人更有优势。 The researchers recently published their findings in a study in the journal Nature Communications. 研究人员最近在《自然通讯》杂志上的一项研究中发表了他们的发现。 Liza Finestack teaches about speech and hearing at the University of Minnesota. 丽莎·芬斯塔克在明尼苏达大学教授语言和听力。 She told The Associated Press (AP) the new study is "a good first step to start looking at the specific genes" that may affect speech and language development. 她告诉美联社(AP),这项新研究是“开始研究可能影响言语和语言发展的特定基因的良好开端”。 Finestack was not involved in the study. 芬斯塔克没有参与这项研究。 Dr. Robert Darnell has long been studying the protein – called NOVA1 – at his laboratory at New York's Rockefeller University. 罗伯特·达内尔博士长期以来一直在他位于纽约洛克菲勒大学的实验室研究这种名为NOVA1的蛋白质。 He helped lead the new research and was a writer of the study. 他帮助领导了这项新研究,并且是这项研究的作者。 Darnell told the AP the genetic version, or variant, included the protein that helped humans develop into the "dominant species" that remains today. 达内尔告诉美联社,基因版本,或变体,包括帮助人类发展成为今天仍然存在的“优势物种”的蛋白质。 The latest research involved scientists using CRISPR gene editing methods to replace the NOVA1 protein found in mice with the one found in humans. 在最新的研究中,科学家们使用CRISPR基因编辑方法,将小鼠体内发现的NOVA1蛋白替换为人类体内发现的NOVA1蛋白。 The aim was to test the real-life effects of the genetic variant. 目的是测试遗传变异对现实生活的影响。 The researchers were surprised to learn that the variant changed the way the animals called out to each other. 研究人员惊讶地发现,这种变异改变了动物相互呼唤的方式。 Baby mice with the human variant made a different sound than normal mice do when their mother came around. 携带人类变异基因的幼鼠在母亲出现时发出的声音与正常小鼠不同。 Adult male mice with the variant also made different sounds when they were near a female they wanted to mate with. 携带这种变异基因的成年雄性老鼠在靠近想要交配的雌性老鼠时,也会发出不同的声音。 Darnell said both of these situations gave the mice a reason to speak. 达内尔说,这两种情况都给了老鼠说话的理由。 Those with the human variant "spoke differently," demonstrating the gene's influence in speech, he added. 他补充说,那些携带人类变异基因的人“说话方式不同”,证明了该基因对语言的影响。 This is not the first time a gene has been linked to speech. 这并不是第一次将基因与语言联系起来。 In 2001, British scientists said they had discovered the first gene tied to a language and speech disorder. 2001年,英国科学家称他们发现了首个与语言障碍有关的基因。 Researchers called this human language gene FOXP2. 研究人员将这个人类语言基因称为FOXP2。 But even though FOXP2 was found to be linked to human language, the variant in modern humans was not found in our species alone. 但是,尽管FOXP2基因被发现与人类语言有关,但现代人类的这种变异并不是只在人类身上发现的。 Later research found it was shared with Neanderthals. 后来的研究发现它与尼安德特人共享。 The NOVA1 variant in modern humans, on the other hand, is found only in our species, Darnell said. 另一方面,现代人类的NOVA1变异只存在于我们这个物种中,达内尔说。 The presence of a gene variant is not the only thing that permits people to speak. 基因变异的存在并不是人类说话的唯一原因。 The ability also depends on physical elements in the human throat and areas of the brain that work together to help people produce speech and understand language. 这种能力还取决于人类喉咙和大脑区域中的物理元素,它们共同作用,帮助人们产生言语和理解语言。 Darnell said he hopes the recent work can lead to new ways to treat speech-related problems. 达内尔说,他希望最近的研究能够为治疗言语相关问题带来新的方法。 The University of Minnesota's Finestack noted the genetic findings could also one day permit scientists to identify people who might need help developing speech and language early in life. 明尼苏达大学的芬斯塔克指出,基因发现有一天还可能使科学家能够识别出哪些人在早期可能需要帮助发展言语和语言。 "That's certainly a possibility," she said. “这当然是有可能的,”她说。 I'm Jill Robbins. 吉尔·罗宾斯为您播报。 |
| 原文地址:http://www.tingroom.com/voa/2025/whys/569170.html |