☆ 4.1 Article

Osteological and Genetic Analysis of the Extinct Ezo Wolf (Canis lupus hattai) from Hokkaido Island, Japan

ZOOLOGICAL SCIENCE (2010)

期刊

ZOOLOGICAL SCIENCE

卷 27, 期 4, 页码 320-324

出版社

ZOOLOGICAL SOC JAPAN

DOI: 10.2108/zsj.27.320

关键词

Canis lupus hattai; genetic variation; mitochondrial DNA; phylogeography

类别

Zoology

资金

Ministry of Education, Science, Sports and Culture, Japan [14405028, 18405034]
Grants-in-Aid for Scientific Research [14405028, 18405034] Funding Source: KAKEN

向作者/读者索取更多资源

Protocol

社区支持

Reagent

社区支持

摘要

The Ezo wolf (Canis lupus hattai Kishida, 1931) is an extinct subspecies that inhabited Hokkaido in Japan until the middle of the Meiji Period. Because there are very few preserved skeletons, no osteological and/or genetic analyses of the Ezo wolf have been conducted. In this study, 20 cranial and eight mandibular characters were measured on Ezo wolf skeletons, and mitochondrial DNA (mtDNA) was analyzed to assess genetic relationships between the Ezo wolf and other wolf lineages, including the Japanese wolf on Honshu. The morphological study showed that the Ezo wolf is larger than the Japanese wolf and similar in size to the grey wolf of the Asian and American Continents. MtDNA control sequences (751 bp) from two Ezo wolves were identical to those from the Canadian grey wolf. The morphological and genetic characters indicate that the ancestor of the Ezo wolf was genetically related to that of the grey wolf in Canada.

作者

我是这篇论文的作者

点击您的名字以认领此论文并将其添加到您的个人资料中。

主要评分

4.1

评分不足

次要评分

新颖性

重要性

科学严谨性

评价这篇论文

TLR7 gain-of-function genetic variation causes human lupus

Grant J. Brown, Pablo F. Canete, Hao Wang, Arti Medhavy, Josiah Bones, Jonathan A. Roco, Yuke He, Yuting Qin, Jean Cappello, Julia I. Ellyard, Katharine Bassett, Qian Shen, Gaetan Burgio, Yaoyuan Zhang, Cynthia Turnbull, Xiangpeng Meng, Phil Wu, Eun Cho, Lisa A. Miosge, T. Daniel Andrews, Matt A. Field, Denis Tvorogov, Angel F. Lopez, Jeffrey J. Babon, Cristina Aparicio Lopez, Africa Gonzalez-Murillo, Daniel Clemente Garulo, Virginia Pascual, Tess Levy, Eric J. Mallack, Daniel G. Calame, Timothy Lotze, James R. Lupski, Huihua Ding, Tomalika R. Ullah, Giles D. Walters, Mark E. Koina, Matthew C. Cook, Nan Shen, Carmen de Lucas Collantes, Ben Corry, Michael P. Gantier, Vicki Athanasopoulos, Carola G. Vinuesa

Summary: Enhanced Toll-like receptor 7 (TLR7) signaling has been associated with human systemic autoimmune disease, but evidence of TLR7 gene variants causing lupus is lacking. In this study, researchers identified a newly described TLR7(Y264H) variant that increased sensing of guanosine and 2',3'-cGMP and was sufficient to cause lupus in mice. Enhanced TLR7 signaling was shown to drive aberrant B cell survival and the accumulation of specific B cell subsets, while deficiency of the downstream adapter protein MyD88 rescued autoimmunity and all phenotypes. The study highlights the importance of TLR7 and guanosine-containing self-ligands in the pathogenesis of lupus and suggests potential therapeutic targets.

NATURE (2022)