Abstract
BackgroundWe have established 17 Y chromosome consomic (Y-consomic) mouse strains in an inbred DH/Sgn strain. In this study, based on investigations in four different genetic backgrounds, we proved that the Y chromosome of the inbred mouse KK/Ta strain is associated with reduced body size.FindingsIn the DH-Chr Y-+/+ background, Y chromosome substitution significantly decreased the body weight in DH-Chr YKK-+/+ and DH-Chr YSJL-+/+ strains, and the DH-Chr YKK-+/+ strain was the lightest among the 17 Y-consomic strains. In the DH-Chr Y-Dh/+ background (Dh/+ mice have skeletal malformations and are usually lighter than +/+ mice), although Y chromosome substitution did not significantly alter the body weight, the DH-Chr YKK-Dh/+ strain was the lightest among the 17 Y-consomic-Dh/+ strains. In the (B6.Cg-Ay × DH-Chr Y) F1-+/+ background, Y chromosome substitution significantly decreased the body weight and length in the (B6.Cg-Ay × DH-Chr YKK) F1 hybrids. In the (B6.Cg-Ay × DH-Chr Y) F1-Ay/+ background (Ay causes obesity and promotes linear growth), Y chromosome substitution significantly decreased body weight and length in the (B6.Cg-Ay × DH-Chr YKK) F1-Ay/+ hybrids.ConclusionA body-size-reducing effect of the Y chromosome of the KK/Ta mouse strain was observed irrespective of genetic background. The effect was observed in the presence of Dh and Ay, the autosomal dominant mutations, both of which are known to have substantial effects on body size. These results suggest that there are Y-linked genes that control the body size in mice.
Highlights
We have established 17 Y chromosome consomic (Y-consomic) mouse strains in an inbred DH/Sgn strain
The effect was observed in the presence of dominant hemimelia (Dh) and Ay, the autosomal dominant mutations, both of which are known to have substantial effects on body size
We identified several SNPs and gene polymorphisms that were associated with testis weight variation when the trait was evaluated as a quantitative trait [2]
Summary
MiceThe following Y-consomic strains were used in this study: DH-Chr YA (Y chromosome from A/J strain), DH-Chr YAKR (AKR/J), DH-Chr YB6 (C57BL/6J), DHChr YBALB (BALB/cA), DH-Chr YC3H (C3H/HeJ), DH-Chr YCAST (CAST/EiJ), DH-Chr YCBA (CBA/N), DH-Chr YCF1 (CF1/Sgn), DH-Chr YDBA (DBA/2J), DHChr YDDD (DDD/Sgn), DH-Chr YDH (identical to DH), DH-Chr YKK (KK/Ta), DH-Chr YRF (RF/J), DH-Chr YRR (RR/Sgn), DH-Chr YSJL (SJL/J), DH-Chr YSS (SS/Sgn), and DH-Chr YSWR (SWR/J). Each Y-consomic strain included Dh/+ and +/+ mice with respect to the genotype at the Dh locus. Dh causes visceral and skeletal malformations of various degrees of severity [3,4]. Visceral abnormalities include a small stomach, short intestine, hydropic kidneys, and congenital absence of the spleen. The skeletal malformations in Dh/+ mice are worth mentioning. Loss of the hallux (i.e., presence of only four digits) is commonly observed in Dh/+ mice. Triphalangy of the hallux (i.e., presence of five digits with an extra phalange on the hallux) is commonly observed. Dh/+ mice were distinguished from +/+ mice by the presence of hindlimb malformation, and the Dh/+ genotype was confirmed by the absence of the spleen on laparotomy
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