著者

Mukai Takahiko Sato Torao Naruse Kiyoshi Inaba Kazuo Shima Akihiro Morisawa Masaaki

出版者

社団法人日本動物学会

雑誌

Zoological science (ISSN:02890003)

巻号頁・発行日

vol.13, no.1, pp.175-183, 1996-02-15

被引用文献数

1

---

The genetic relationships and taxonomic status of 7 taxa belonging to the genus Tridentiger (Pisces, Gobiidae) were investigated by means of analysis of allozymic variation at 14 loci. The results suggest that the two taxa "T. obscurus" and "T. brevispinis" which are sympatric and morphologically similar are reproductively isolated and are highly divergent from each other (the genetic distance values are 0.501-0.707). It is also suggested that "T. brevispinis" and "T. kuroiwae" are genetically different enough from each other to deserve subspecies at least. The other 4 taxa, "T. barbatus", "T. nudicervicus", "T. trigonocephalus" and "T. bifasciatus", are genetically divergent each and are considered to be 4 biological species. A dendrogram showing the phylogenetic relationships of the 7 taxa was constructed from the genetic distances.

著者

Uemura Norihito Koike Masato Ansai Satoshi Kinoshita Masato Ishikawa-Fujiwara Tomoko Matsui Hideaki Naruse Kiyoshi Sakamoto Naoaki Uchiyama Yasuo Todo Takeshi Takeda Shunichi Yamakado Hodaka Takahashi Ryosuke

出版者

Public Library of Science

雑誌

PLOS genetics (ISSN:15537404)

巻号頁・発行日

vol.11, no.4, 2015-04-02

被引用文献数

59

---

パーキンソン病の解明に役立つメダカの作製に成功 -メダカが神経変性疾患の研究に貢献できる可能性- 京都大学プレスリリース. 2015-04-09.Homozygous mutations in the glucocerebrosidase (GBA) gene result in Gaucher disease (GD), the most common lysosomal storage disease. Recent genetic studies have revealed that GBA mutations confer a strong risk for sporadic Parkinson's disease (PD). To investigate how GBA mutations cause PD, we generated GBA nonsense mutant (GBA-/-) medaka that are completely deficient in glucocerebrosidase (GCase) activity. In contrast to the perinatal death in humans and mice lacking GCase activity, GBA-/- medaka survived for months, enabling analysis of the pathological progression. GBA-/- medaka displayed the pathological phenotypes resembling human neuronopathic GD including infiltration of Gaucher cell-like cells into the brains, progressive neuronal loss, and microgliosis. Detailed pathological findings represented lysosomal abnormalities in neurons and alpha-synuclein (α-syn) accumulation in axonal swellings containing autophagosomes. Unexpectedly, disruption of α-syn did not improve the life span, formation of axonal swellings, neuronal loss, or neuroinflammation in GBA-/- medaka. Taken together, the present study revealed GBA-/- medaka as a novel neuronopathic GD model, the pahological mechanisms of α-syn accumulation caused by GCase deficiency, and the minimal contribution of α-syn to the pathogenesis of neuronopathic GD.