Expression analysis of P/Q-type Ca2+ channel alpha 1A subunit mRNA in olfactory mitral cell in N-type Ca2+ channel alpha 1B subunit gene-deficient mice.
N-type and P/Q-type Ca2+ channels play an important role in the processing of olfactory information. However, N-type Ca2+ channel alpha1B-deficient mice show normal behavior, presumably owing to compensation by other Ca2+ channels. P/Q-type Ca2+ channel alpha1A mRNA was expressed at a higher level in olfactory bulb of homozygous alpha1B-deficient mice than wild-type or heterozygous mice. LacZ expression in olfactory mitral cells of homozygous alpha1B-deficient x alpha1A1.5-lacZ mice, carrying a 1.5-kb 5'-upstream fragment of the alpha1A gene fused to the lacZ reporter gene, was increased compared to that in wild-type or heterozygous mice. Therefore, a possible explanation for the normal behavior of alpha1B-deficient mice is compensation by the alpha1A gene and that the 1.5-kb 5'-upstream region of this gene contains an enhancer cis-element for compensation in olfactory mitral cells.
Takahashi
Eiki
E
Tsukuba Research Laboratory, Eisai Co. Ltd., 5-1-3 Tokodai, Tsukuba, Ibaraki 300-2635, Japan. e2-takahashi@hhc.eisai.co.jp
Ino
Mitsuhiro
M
Miyamoto
Norimasa
N
Nagasu
Takeshi
T
D000818:Animals; D015220:Calcium Channels / Q000096:biosynthesis* / Q000235:genetics / Q000502:physiology; D020864:Calcium Channels, N-Type / Q000096:biosynthesis / Q000172:deficiency / Q000235:genetics; D020865:Calcium Channels, P-Type; D020907:Calcium Channels, Q-Type; D005786:Gene Expression Regulation / Q000502:physiology; D051379:Mice; D008810:Mice, Inbred C57BL; D008808:Mice, Inbred CBA; D018345:Mice, Knockout; D009830:Olfactory Bulb / Q000166:cytology* / Q000378:metabolism*; D012333:RNA, Messenger / Q000096:biosynthesis* / Q000235:genetics; D001616:beta-Galactosidase / Q000096:biosynthesis
D015220:Calcium Channels; D020864:Calcium Channels, N-Type; D020865:Calcium Channels, P-Type; D020907:Calcium Channels, Q-Type; D012333:RNA, Messenger; D001616:beta-Galactosidase