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瘦素受体基因对猪体重的母体拮抗效应和直接效应

Antagonistic maternal and direct effects of the leptin receptor gene on body weight in pigs.

作者信息

Solé Emma, Ros-Freixedes Roger, Tor Marc, Reixach Josep, Pena Ramona N, Estany Joan

机构信息

Department of Animal Science, University of Lleida-Agrotecnio Center, Lleida, Catalonia, Spain.

Selección Batallé S.A., Riudarenes, Catalonia, Spain.

出版信息

PLoS One. 2021 Jan 28;16(1):e0246198. doi: 10.1371/journal.pone.0246198. eCollection 2021.

DOI:10.1371/journal.pone.0246198
PMID:33508034
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7842917/
Abstract

Maternal effects on offspring growth can impact survival and evolution of natural and domesticated populations. Genetic correlation estimates often support a negative relationship between direct and maternal effects. However, the genetic underpinnings whereby this antagonism operates are unclear. In pigs, sow feeding status and body composition condition piglet development and growth. We hypothesized that variants in genes impacting these traits may be causative of maternal influences that could be antagonistic to the direct effects for piglet growth. A recessive missense mutation (C>T) in the porcine leptin receptor (LEPR) gene (rs709596309) has been identified as the possible causal polymorphism for increased feed intake and fatness. Using data from a Duroc line, we show that the TT sows exerted a negative impact on the body weight of their offspring at the end of the growing period of similar extent to the positive direct effect of the TT genotype over each individual. Thus, TT pigs from TT dams were about as heavy as CC and CT (C-) pigs from C-dams, but TT pigs from C-dams were around 5% heavier than C-pigs from TT dams. In contrast, body composition was only influenced by LEPR direct effects. This antagonism is due to a higher propensity of TT pigs for self-maintenance rather than for offspring investment. We show that TT pigs consumed more feed, favored fatty acid uptake over release, and produced lighter piglets at weaning than their C-counterparts. We conclude that LEPR underlies a transgenerational mechanism for energy distribution that allocates resources to the sow or the offspring according to whether selective pressure is exerted before or after weaning.

摘要

母体对后代生长的影响会影响自然种群和驯化种群的生存与进化。遗传相关性估计通常支持直接效应和母体效应之间的负相关关系。然而,这种拮抗作用产生的遗传基础尚不清楚。在猪中,母猪的饲养状况和身体组成会影响仔猪的发育和生长。我们假设,影响这些性状的基因变异可能是母体影响的原因,而这种影响可能与仔猪生长的直接效应相互拮抗。猪瘦素受体(LEPR)基因(rs709596309)中的一个隐性错义突变(C>T)已被确定为饲料摄入量增加和肥胖的可能因果多态性。利用杜洛克品系的数据,我们发现,TT基因型母猪对其后代生长期末体重的负面影响程度,与TT基因型对每个个体的正向直接效应相当。因此,来自TT基因型母猪的TT仔猪体重与来自C基因型母猪的CC和CT(C-)仔猪相近,但来自C基因型母猪的TT仔猪比来自TT基因型母猪的C仔猪重约5%。相比之下,身体组成仅受LEPR直接效应的影响。这种拮抗作用是由于TT仔猪更倾向于自我维持而非对后代的投入。我们发现,TT仔猪比其C基因型对照消耗更多饲料,更倾向于脂肪酸摄取而非释放,并且断奶时产仔较轻。我们得出结论,LEPR是一种跨代能量分配机制的基础,该机制根据断奶前后是否施加选择压力,将资源分配给母猪或后代。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/33bc/7842917/7a952cadf7c9/pone.0246198.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/33bc/7842917/80f5125ee47b/pone.0246198.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/33bc/7842917/7a952cadf7c9/pone.0246198.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/33bc/7842917/80f5125ee47b/pone.0246198.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/33bc/7842917/7a952cadf7c9/pone.0246198.g002.jpg

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