Changes in temperature preferences and energy homeostasis in dystroglycan mutants

Science

Volumn 323, Issue 5922, 2009, Pages 1740-1743

  Takeuchi, Ken Ichi ^a,b   Nakano, Yoshiro ^c   Kato, Utako ^a   Kaneda, Mizuho ^b   Aizu, Masako ^b   Awano, Wakae ^d   Yonemura, Shigenobu ^e   Kiyonaka, Shigeki ^a   Mori, Yasuo ^a   Yamamoto, Daisuke ^f   Umeda, Masato ^a,b  

^a KYOTO UNIVERSITY   (Japan)

^b TOKYO METROPOLITAN INSTITUTE OF MEDICAL SCIENCE   (Japan)

^c HYOGO COLLEGE OF MEDICINE   (Japan)

^d MITSUBISHI KASEI INST OF LIFE SCI   (Japan)

^e RIKEN Center for Biosystems Dynamics Research   (Japan)

^f TOHOKU UNIVERSITY   (Japan)

Author keywords

[No Author keywords available]

Indexed keywords

DYSTROGLYCAN;

EVOLUTIONARY BIOLOGY; FLY; GENE EXPRESSION; HOMEOSTASIS; METABOLISM; MITOCHONDRIAL DNA; MUTATION; PHENOTYPE; TEMPERATURE EFFECT; THERMOREGULATION;

AEROBIC METABOLISM; ARTICLE; BODY TEMPERATURE; COLD TOLERANCE; CONTROLLED STUDY; DROSOPHILA MELANOGASTER; ENERGY BALANCE; HOMEOSTASIS; LOW TEMPERATURE; MITOCHONDRION; MUTAGENESIS; MUTANT; NONHUMAN; PHENOTYPE; PRIORITY JOURNAL; PROTEIN EXPRESSION; THERMOGENESIS; THERMOREGULATION;

ADENOSINE TRIPHOSPHATE; ANIMALS; ANIMALS, GENETICALLY MODIFIED; BODY TEMPERATURE REGULATION; CALCIUM; COLD TEMPERATURE; DROSOPHILA MELANOGASTER; DROSOPHILA PROTEINS; DYSTROGLYCANS; ENERGY METABOLISM; HOMEOSTASIS; MITOCHONDRIA; MUTANT PROTEINS; MUTATION; OXYGEN CONSUMPTION; PHENOTYPE; PYRUVATE DEHYDROGENASE COMPLEX; TEMPERATURE;

ANIMALIA;

EID: 63449090607     PISSN: 00368075     EISSN: 10959203     Source Type: Journal    
DOI: 10.1126/science.1165712     Document Type: Article

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20. Wild type, 7.3 ± 1.8% (mean ± SEM); atu mutant, 67.3 ± 3.7%; and DmDG transgenic atu mutant (atu/atu; actin5C-GAL4/UAS-DmDG), 7.3 ± 1.8%. Error bars represent SEM (n = 3).
21. Control actin5C-GAL4 line (actin5C-GAL4/+), 15.7 ± 4.2% (mean ± SEM); "DmDG-knockdown" line (actin5C-GAL4/UAS- dsRNA), 59.0 ± 3.6%; and control UAS-dsRNA line (+IUAS-dsRNA), 25.4 ± 7.7%. Error bars represent SEM (n = 7).
22. Wild type, 1.6 : 0.1 (mean ± SEM); atu mutant, 3.0 x 0.1; and DmDG-transgenic atu mutant (atu/atu; actin5C-GAL4/UAS-DmDG), 2.2 : 0.2. Error bars represent SEM (n = 6).
23. Wild type, 20.9 ± 1.5 (mean = SEM; n = 9); atu mutant, 27.0 ± 1.8 (n = 8); and DmDG-transgenic atu mutant (atu/atu; actin5C-GAL4/UAS-DmDG), 20.2 : 1.2 (n = 8).
24. Wild type, 15.7 = 0.4 (mean = SEM); atu mutant, 32.3 ± 1.8; and DmDG-transgenic atu mutant (atu/atu; aetin5C-GAL4/UAS-DmDG), 25.2 ± 1.6 (n = 3).
25. Wild type, 124.9 ± 1.9 (mean = SEM; n = 202); atu mutant, 148.5 ± 2.3 (n = 194); and DmDG-transgenic atu mutant (atu/atu; actin5C-GAL4/UAS-DmDG), 115.5 ± 2.9 (n = 119).
26. Wild type, 139.0 ± 4.7 (mean : SEM; n = 98); atu mutant, 151.8 : 7.4 (n = 88); and DmDG-transgenic atu mutant (atu/atu; actin5C-GAL4/UAS- DmDG), 101.9 = 6.3 (n = 79).
27. We thank Y. Nakano for statistical analysis; H. Suzuki and J. Ikenouchi for assistance with electron microscopy; R. Niwa, M. O'Connor, A. P. Gould, and M. Kamakura for providing GAL4 flies; N. Juni for helpful discussions; A. Yamaguchi, Y. Yamaguchi, and M. Nishikawa for technical assistance; and R. Matsuda, H. Takeshima, Y. Nagai, and M. Ui for valuable advice and encouragement. This work was supported in part by Special Coordination Funds for Promoting Science and Technology from MEXT (Ministry of Education, Culture, Sports, Science and Technology), Japan, and by a research grant from The Novartis Foundation (Japan) for the Promotion of Science. D.Y. was supported by Specially Promoted Research grant 1802012 from MEXT and The Tohoku Neuroscience Global Centers of Excellence program.