RT Journal Article
SR Electronic
T1 Genetics of mouse behavioral and peripheral neural responses to sucrose
JF bioRxiv
FD Cold Spring Harbor Laboratory
SP 2020.08.19.253989
DO 10.1101/2020.08.19.253989
A1 Cailu Lin
A1 Masashi Inoue
A1 Xia Li
A1 Natalia P. Bosak
A1 Yutaka Ishiwatari
A1 Michael G. Tordoff
A1 Gary K. Beauchamp
A1 Alexander A. Bachmanov
A1 Danielle R. Reed
YR 2020
UL http://biorxiv.org/content/early/2020/08/19/2020.08.19.253989.abstract
AB Mice of the C57BL/6ByJ (B6) strain have higher consumption of, and stronger peripheral neural responses to, sucrose solution than do mice of the 129P3/J (129) strain. To identify quantitative trait loci (QTLs) responsible for this strain difference and evaluate the contribution of peripheral taste responsiveness to individual differences in sucrose intake, we produced an intercross (F2) of 627 mice, measured their sucrose consumption in two-bottle choice tests, recorded the electrophysiological activity of the chorda tympani nerve elicited by sucrose in a subset of F2 mice, and genotyped the mice with DNA markers distributed in every mouse chromosome. We confirmed a sucrose consumption QTL (Scon2, or Sac) on mouse chromosome (Chr) 4, harboring the Tas1r3 gene, which encodes the sweet taste receptor subunit T1R3 and affects both behavioral and neural responses to sucrose. For sucrose consumption, we also detected five new main-effect QTLs Scon6 (Chr2), Scon7 (Chr5), Scon8 (Chr8), Scon3 (Chr9) and a sex-specific QTL Scon9 (Chr15), and an interacting QTL pair Scon4 (Chr1) and Scon3 (Chr9). No additional QTLs for the taste nerve responses to sucrose were detected besides the previously known one on Chr4 (Scon2). Identification of the causal genes and variants for these sucrose consumption QTLs may point to novel mechanisms beyond peripheral taste sensitivity that could be harnessed to control obesity and diabetes.Competing Interest StatementThe authors have declared no competing interest.