Annual Drosophila research conference, 2011.
Annual Drosophila research conference, 2011.
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年度果蝇研究会议，2011。
DOI：
10.1002/dvdy.22689
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发表时间：
2011
期刊：
影响因子：
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通讯作者：
Singh,Amit
中科院分区：
文献类型：
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作者：
Call,GeraldB;Verghese,Shilpi;Puli,OorvashiRoy;Hemmerle,DawnM;Kango-Singh,Madhuri;Singh,Amit
美丽的圣地亚哥，以美国第八大城市圣迪达克斯(西班牙语：San Diego de Alcalá)命名的城市，是第52届年度果蝇研究会议的举办地。圣地亚哥市拥有壮观的风景，有数英里的海滨海滩、海湾潮滩、峡谷、山脉和沙漠。这次会议由美国遗传学会(GSA)主办，由纽约康奈尔大学的Daniel Barbash、亚利桑那大学的Giovanni Bosco和马萨诸塞州Brandeis大学的Leslie Griffith组织。这次年会汇聚了来自世界各地的基础研究科学家，他们研究遗传模式生物--常见的果蝇--黑腹果蝇。今年的会议取得了巨大成功，有900个海报演示、156个平台会议、14个全体会议、12个研讨会和16个展品。开幕式以GSA前主席(2010年)Scott Hawley(密苏里州斯托尔斯医学研究所)介绍GSA的最新期刊G3开始。这本杂志将是发表基础的、基于序列的、基于屏幕的等重要遗传学研究的地方。他继续向约翰·卡尔森(耶鲁大学，康涅狄格州)颁发GSA奖章，以表彰他在过去15年中在遗传学领域的杰出贡献，以表彰他在嗅觉遗传学方面的工作。诺贝尔奖获得者约翰·卡尔森负责解开嗅觉之谜，是嗅觉领域的先驱。他帮助发现了一个由60个气味感受器组成的家族，表达在果蝇的触角和上颌触须上。拉里·桑德勒纪念奖颁发给丹尼尔·巴布科克(Daniel Babcock)，他是德克萨斯州MD Anderson癌症中心的Michael Galko实验室博士，他的论文是关于果蝇幼虫的伤害性感受。他首先将超感痛症定义为伤害性刺激(伤害性刺激是实际或潜在的组织损害事件)的降低阈值，而痛敏则定义为对伤害性刺激的夸大反应。这些都是有助于促进伤害保护的有用条件。然而，如果他们坚持下去，他们可能会让人虚弱。传统观点认为，痛觉异常和痛觉过敏都是由相同的机制发生的。然而，通过一系列优雅的实验，他的研究表明，这两种情况是分开的。他们用紫外线(UV)交联剂引起组织损伤，而不影响生存能力。紫外线照射24小时后，表皮明显受损，而负责伤害性感受的神经元没有受到影响。这一模型在幼虫中既引起了痛觉过敏又引起了痛觉过敏。在紫外线刺激后阻止表皮细胞的凋亡可以阻止痛觉过敏。因此，垂死的表皮细胞会释放一些导致痛觉过敏的因素。他们发现，Eiger(EGR，果蝇肿瘤坏死因子，TNF)突变的果蝇不会出现紫外线损伤的痛觉过敏。有趣的是，EGR突变体对痛觉过敏反应没有任何影响。这是第一次对痛觉过敏症和痛觉过敏进行基因解剖。这次会议的历史讲座小组讨论了果蝇的行为研究。马萨诸塞州布兰迪斯大学的Michael Rosbash讨论了这一研究领域的总体历史。他讨论了西摩·本泽、马丁·海森伯格和比尔·帕克是如何开创这一领域的。他讨论了有关昼夜节律的工作。
Beautiful San Diego, a city named after Saint Didacus (Spanish: San Diego de Alcalá), the eighth largest city of United States, was the location of the 52nd Annual Drosophila Research Conference. The city of San Diego boasts a spectacular landscape with miles of oceanfront beaches, bayfront tidelands, canyons, mountains, and deserts. The meeting was sponsored by the Genetics Society of America (GSA) and was organized by Daniel Barbash (Cornell University, New York), Giovanni Bosco (University of Arizona), and Leslie Griffith (Brandeis University, Massachusetts). This annual meeting brings together basic research scientists from all over the world, who study the genetic model organism, Drosophila melanogaster, the common fruit fly. This year’s meeting was a huge success with 900 poster presentations, 156 platform sessions, 14 plenary sessions, 12 workshops, and 16 exhibits. The opening session started off with the past president (2010) of the GSA, Scott Hawley (Stowers Institute for Medical Research, Missouri) introducing the newest journal of the GSA, G3. This journal will be a place to publish important genetics research that is fundamental, sequence-based, screen-based, etc. He continued by presenting the GSA medal for outstanding contributions in the field of genetics in the last 15 years to John Carlson (Yale University, Connecticut) for his work on the genetics of olfaction. John Carlson, a Nobel laureate, is responsible for solving the mystery of smell and has been a pioneer in the field of olfaction. He has been instrumental in discovering a family of 60 odorant receptors expressed in the antennae and the maxillary palps of Drosophila. The Larry Sandler Memorial Award was presented to Daniel Babcock (Dr. Michael Galko Lab, MD Anderson Cancer Center, Texas) on his dissertation on nociception in Drosophila larvae. He began by defining allodynia as a lowered threshold for a noxious stimulus (a noxious stimulus is an actual or potential tissue damaging event) and hyperalgesia as an exaggerated response to a noxious stimulus. These are useful conditions to help foster injury protection. However, if they persist, they can be debilitating. The traditional view has accepted that both allodynia and hyperalgesia occur by the same mechanism. However, through an elegant series of experiments, his research showed that these two conditions are separate. They elicited tissue damage with an ultraviolet (UV) crosslinker without affecting viability. Twenty-four hours after UV exposure, the epidermis had marked damage, while the neurons responsible for nociception were unaffected. This model caused both allodynia and hyperalgesia in the larvae. Blocking apoptosis in the epidermal cells following the UV stimulus blocks allodynia. Therefore, the dying epidermal cells release some factor that causes allodynia. They found that flies mutant for eiger (egr, Drosophila tumor necrosis factor, TNF) cannot develop allodynia with UV damage. Of interest, egr mutants did not have any effect on the hyperalgesia response. This was the first genetic dissection of allodynia and hyperalgesia. The historical lecture panel of this conference discussed behavioral studies in Drosophila. Michael Rosbash (Brandeis University, Massachusetts) discussed the overall history of this area of research. He discussed how Seymour Benzer, Martin Heisenberg, and Bill Pak started the whole field. He discussed the work on circadian