J亚群禽白血病是由ALV-J引起的一种肿瘤性疾病，严重危害养禽业。本团队通过培育对ALV-J具有高抗性的鸡，并从中筛选到一个重要的抗病基因——GADD45β，该基因主要参与调控细胞增生、细胞周期、细胞凋亡和DNA损伤修复。研究发现ALV-J可通过抑制细胞自噬来促进病毒增殖，而GADD45β在细胞自噬过程中发挥负调控作用，且与ALV-J病毒复制密切相关。基于这些研究基础，本项目将深入研究GADD45β对ALV-J抑制细胞自噬的调控机制，探讨GADD45β调控MEKK4-p38MAPK信号通路对ALV-J抑制细胞自噬的影响，阐明GADD45β通过促进细胞自噬实现其抗ALV-J病毒感染的作用机制；同时研究GADD45β异常甲基化与表达量的关系，探讨GADD45β在ALV-J抗性鸡中高表达是否与该基因本身的异常甲基化有关。本项目研究成果对J亚群禽白血病的防控和抗病育种有重要的理论和实践意义。

Subgroup J avian leukosis cause by subgroup J avian leukosis virus (ALV-J) is infectious neoplastic disease which has been seriously plaguing poultry industry. Our team is breeding purebred chicken with high ALV-J resistance in which we filtrate an essential anti-disease gene — GADD45β for study. This gene mainly involves in the courses of repairing DNA damage, and regulating cell proliferation , cell cycle and cell apoptosis. It has been proved by some research results that ALV-J can promote cell proliferation via inhibiting cell autophagy and that GADD45β exerts negative impacts on regulating the process of cell autophagy, which apparently demonstrates the intimate connection between GADD45β and ALV-J proliferation. Based on these research results, our project is to conduct thorough researches to precisely probe into the mechanism of how GADD45 regulates the cell autophagy inhibiting process of ALV-J, elaborately explore what impacts GADD45β could inflict on cell autophagy inhibiting effect of ALV-J through regulating MEKK4-p38MAPK signal path way, and further illuminate the GADD45β’s anti-ALV-J mechanism which functions through promoting cell autophagy. At the same time our group aims to study the relationship between abnormal methylation and expression of GADD45β, focusing on whether the abnormal methylation of this gene is related to its high expression in chicken with high ALV-J resistance. Our research achievements will definitely have an important theoretical and practical meaning in subgroup J avian leukosis prevention and chicken breeding with such disease resistance.