Four dominant loci for the vascular responses by the antitumor polysaccharide, lentinan
Maeda, Y.Y.; Takahama, S.; Yonekawa, H.
Immunogenetics 47(2): 159-165
1998
ISSN/ISBN: 0093-7711
PMID: 9396862
DOI: 10.1007/s002510050341
Accession: 008701666
Lentinan, beta-1,6;1,3-glucan, showing an antitumor effect against mouse solid type tumors, can induce marked vascular dilation and hemorrhage (VDH) in very localized areas such as the ears, feet, and tails of mice in the early stages after its administration (Maeda et al. 1984). VDH has been found to be one of the T-cell-mediated responses triggered by lentinan. We reported previously that the responsiveness of mice to lentinan with respect to VDH induction is controlled by a dominant gene(s), Ltn2 (formerly), and that no sex difference was observed (Maeda et al. 1991). To determine the chromosomal location of the Ltn2 gene(s), we typed genomic DNAs of 193 N2 segregants of crosses between a high responder MA/MyJ and a low responder AKR/J by the polymerase chain reaction-simple sequence length polymorphism technique using 83 chromosome-specific microsatellite markers. We identified one major gene (Ltnr3) and three minor genes (Ltnr4, Ltnr5, and Ltnr6) responsible for the VDH induction. Ltnr3 was closely linked to D6Mit135 on chromosome 6 (P <0.00000) and Ltnr4, Ltnr5, and Ltnr6 to D9Mit161 on chromosome 9 (P <0.00032), D15Mit147 on chromosome 15 (P <0.00014) and D16Mit4 on chromosome 16 (P <0.00014), respectively.