脂肪的过量沉积严重影响了肉鸡生产。而母源性共轭亚油酸（CLA）可降低雏鸡体脂沉积，但其机制尚不清楚。研究显示，CLA介导的脂肪细胞去脂化依赖于磷脂酶C（PLC）对胞内钙离子[Ca2+]i和ERK1/2的激活。我们在预实验中发现，母源性CLA上调了鸡胚PLC、CaMKII、ERK1/2的表达，抑制了PPARγ表达；在体外，PLC抑制剂削弱了CLA介导的CaMKII、ERK1/2的激活，并促进了PPARγ表达和脂滴沉积。因此我们推测母源性CLA通过激活PLC/Ca2+-ERK1/2通路抑制鸡胚成脂分化。为验证该假说，我们将分别以CLA富集种蛋孵育的鸡胚和鸡前脂肪细胞为动物和细胞模型，运用siRNA、PLCγ1转染、双荧光素酶报告、激光共聚焦等技术，借助PLC、[Ca2+]i、ERK1/2抑制剂，从整体-组织-细胞层次揭示母源性CLA抑制鸡胚成脂分化的机制，为解决肉鸡腹脂过量沉积问题提供新思路。

Excessive fat depots severely affected broiler production. It has been reported that maternal conjugated linoleic acid (CLA) supplementation reduced fat accumulation in offspring broilers, but the mechanisms are still unclear. Several studies showed that CLA-mediated adipocyte deplication is dependent on the activation of phospholipase C (PLC), which triggers intracellular calcium accumulation and ERK1/2 pathway activity. In our previus study, we demonstrated that maternal CLA increased the expression of PLCγ1, CaMKII (the downstream activator of [Ca2+]i) and ERK1/2, and decreased the expression of PPARγ mRNA in adipose tissue of chick embryo. In vitro, PLC inhibitor attentuated CLA-mediated activation of CaMKII and ERK1/2, and suppression of PPARγ expression and lipid droplet deposition in preadipocytes. Therefore, we hypothesize that maternal CLA inhibits chick embryo adipogenesis by activating PLC/Ca2+-ERK1/2 pathways. To test the hypothesis, the chick embryos from CLA enriched eggs and chicken preadipocytes are used to establish animal and cell models respectively. We aim to reveal the mechanism of maternal CLA inhibiting chick embryo adipogenesis through the overal level, tissue level andcellular level, by using multiple molecular biology technologies, such as siRNA, PLCγ1 transfection, double luciferase report system and laser confocal, and several specific inhibitors of PLCγ1, [Ca2+]i and ERK1/2. This study provides a new way for reducing fat deposition in broiler production.