肌肉分化主要指成肌细胞向肌管转化的过程，该过程可影响肌纤维的数量和粗细，是决定动物产肉潜力的关键。为挖掘可调控该过程的遗传因子，我们前期对家鸡成肌细胞和肌管进行三代全长转录组测序，发现一种“尾对尾”式天然反义转录本（TtT-NAT）广泛存在于调控肌肉分化的标记基因中。这类反义转录本只占所有天然反义转录本的5.06%，但却集中表达于影响肌肉分化的关键基因中，而且还表现出肌肉特异表达、分化期上调表达、“尾对尾”区域能与正义转录本形成dsRNA的特点，猜测它们可能通过影响正义转录本表达，调控家鸡肌肉发育。本项目将以调控肌肉分化标记基因的MyoNATs为研究对象，检测它们对家鸡肌肉发育的作用，找出决定它们表达的调控机制，阐述它们的作用机理，并探讨TtT-NAT在细胞分化中的生物学意义。项目的实施不仅对提升家鸡产肉潜力具有理论意义，而且可拓展天然反义转录本的作用方式，发掘出新的基因表达调控机制。

Muscle differentiation mainly refers to the process of myoblasts transforming into myotubes. This process can affect the number and size of muscle fibers and is the key to determine the meat production potential of animals. In order to discover the genetic factors that can regulate muscle differentiation, we sequenced the transcriptomes of chicken myoblasts and myotubes by using single-molecule full-length transcript sequencing. We found that many tail-to-tail natural antisense transcripts (TtT-NATs) were expressed in muscle differentiation marker genes. TtT-NATs account for only 5.06% of all natural antisense transcripts, but they are concentrated express in the key genes affecting muscle differentiation. Additionally, these TtT-NATs were muscle-specific expression, and they would up-regulated their expression during muscle differentiation. The “tail-to-tail” region of the TtT-NATs can form dsRNA with the corresponding sense transcript. Therefore, we suppose that the TtT-NATs can regulate chicken muscle development by interacting with their sense transcripts. This study will focus on the MyoNATs, which can regulate the muscle differentiation marker genes. We will detect the functions of MyoNATs in chicken muscle development, find out the regulatory mechanism that determines their expression, elaborate their mechanism of action, and explore the biological significance of TtT-NATs during cell development. The implementation of this study not only has theoretical significance to enhance the meat production potential of domestic chickens, but also can expand the roles of natural antisense transcript and find out new gene expression regulation mechanism.