The loss of conserved genes has the potential to alter phenotypes drastically. Screening of vertebrate genomes for lineage-specific gene loss events has identified numerous natural knockouts associated with specific phenotypes. We provide evidence for the loss of a multi-exonic plasminogen receptor KT (PLGRKT) protein-encoding gene located on the Z chromosome in chicken. Exons 1 and 2 are entirely missing; remnants of exon 3 and a mostly intact exon 4 are identified in an assembly gap-free region in chicken with conserved synteny across species and verified using transcriptome and genome sequencing. PLGRKT gene disrupting changes are present in representative species from all five galliform families. In contrast to this, the presence of an intact transcriptionally active PLGRKT gene in species such as mallard, swan goose, and Anolis lizard suggests that gene loss occurred in the galliform lineage sometime between 68 and 80 Mya. The presence of galliform specific chicken repeat 1 (CR1) insertion at the erstwhile exon 2 of PLGRKT gene suggests repeat insertion-mediated loss. However, at least nine other independent PLGRKT coding frame disrupting changes in other bird species are supported by genome sequencing and indicate a role for relaxed purifying selection before CR1 insertion. The recurrent loss of a conserved gene with a role in the regulation of macrophage migration, efferocytosis, and blood coagulation is intriguing. Hence, we propose potential candidate genes that might be compensating the function of PLGRKT based on the presence of a C-terminal lysine residue, transmembrane domains, and gene expression patterns.

保守基因的丢失可能会大大改变表型。筛选脊椎动物基因组的谱系特异性基因丢失事件已确定了与特定表型相关的众多自然敲除。我们提供了位于鸡Z染色体上的多外显子纤溶酶原受体KT（PLGRKT）蛋白质编码基因丢失的证据。第1和第2外显子完全缺失。在鸡中无装配缺口的区域中鉴定出外显子3和大部分完整的外显子4的残基，跨物种的保守性相同，并使用转录组和基因组测序进行了验证。PLGRKT基因破坏性变化存在于所有五个鸡形目家族的代表性物种中。与此相反，存在完整的转录活性绿头鸭，天鹅鹅和蜥蜴等物种的PLGRKT基因表明，基因丢失发生在68至80 Mya的鸡形谱系中。在PLGRKT基因的先前第2外显子上存在鸡形特异性鸡重复序列1（CR1），提示重复插入介导的丢失。但是，基因组测序支持至少九个其他独立的PLGRKT编码框架破坏其他鸟类的变化，它们支持基因组测序，并表明在CR1插入之前放松纯化选择的作用。有趣的是，一个保守基因的反复缺失引起了巨噬细胞的迁移，红细胞增多和凝血功能的调节。因此，我们提出可能补偿PLGRKT功能的潜在候选基因 基于C端赖氨酸残基，跨膜结构域和基因表达模式的存在。