Northern blot analysis was conducted with mitochondrial RNA from seedling leaves, floral buds, and developing seeds of NCa CMS, maintainer line and fertile F1 using ten mitochondrial genes as probes. The results revea...Northern blot analysis was conducted with mitochondrial RNA from seedling leaves, floral buds, and developing seeds of NCa CMS, maintainer line and fertile F1 using ten mitochondrial genes as probes. The results revealed that 9 out of the 10 mitochondrial genes, except for atp6, showed no difference in different tissues of the corresponding materials of NCα CMS system and that they might be constitutively expressed genes. Eight genes, such as orf139, orf222, atpl, cox1, cox2, cob, rm5S, and rm26S, showed no difference among the three tissues of all the materials detected. So the expression of these eight genes was not regulated by nuclear genes and was not tissue-specific. The transcripts of atp9 were identical among different tissues, but diverse among different materials, indicating that transcription of atp9 was neither controlled by nuclear gene nor tissue-specific. Gene atp6 displayed similar transcripts with the same size among different tissues of all the materials but differed in abundance among tissues of corresponding materials and its expression might be tissue-specific under regulation of nuclear gene. Moreover, three transcripts of orf222 were detected in the floral buds of NCa cms and fertile F1, but no transcript was detected in floral buds of the maintainer line.The transcription of orf139 was similar to that of orf222 but only two transcripts of 0.8 kb and 0.6 kb were produced. The atp9 probe detected a single transcript of 0.6 kb in NCa cms and in maintainer line and an additional transcript of 1.2 kb in fertile F1. The relationship of expression of orf222, orf139, and atp9 with NCa sterility was discussed.展开更多
程序化细胞死亡蛋白-1(programmed cell death protein-1, PD-1)是一个由Pdcd1编码的抑制性辅助受体(co-inhibitory receptor),它对T细胞的免疫应答具有重要的调节作用。PD-1信号通路在急性感染过程中可以防止T细胞的过度激活,但是在慢...程序化细胞死亡蛋白-1(programmed cell death protein-1, PD-1)是一个由Pdcd1编码的抑制性辅助受体(co-inhibitory receptor),它对T细胞的免疫应答具有重要的调节作用。PD-1信号通路在急性感染过程中可以防止T细胞的过度激活,但是在慢性感染过程中可以引起T细胞耗竭(T cell exhaustion)。肿瘤浸润T细胞(tumor-infiltrating T cells)高表达PD-1可以导致肿瘤细胞的免疫逃逸,靶向PD-1信号通路的免疫治疗已经在肿瘤治疗方面取得了巨大的成功。Pdcd1在免疫细胞中的表达存在复杂的调控机制,本文将对这方面的研究进展作一综述。展开更多
基金This work was supported by the National High Technology R&D Project of China (No.2002AA207009) and Wuhan Dawn Project for Youth (No. 20035002016-36).
文摘Northern blot analysis was conducted with mitochondrial RNA from seedling leaves, floral buds, and developing seeds of NCa CMS, maintainer line and fertile F1 using ten mitochondrial genes as probes. The results revealed that 9 out of the 10 mitochondrial genes, except for atp6, showed no difference in different tissues of the corresponding materials of NCα CMS system and that they might be constitutively expressed genes. Eight genes, such as orf139, orf222, atpl, cox1, cox2, cob, rm5S, and rm26S, showed no difference among the three tissues of all the materials detected. So the expression of these eight genes was not regulated by nuclear genes and was not tissue-specific. The transcripts of atp9 were identical among different tissues, but diverse among different materials, indicating that transcription of atp9 was neither controlled by nuclear gene nor tissue-specific. Gene atp6 displayed similar transcripts with the same size among different tissues of all the materials but differed in abundance among tissues of corresponding materials and its expression might be tissue-specific under regulation of nuclear gene. Moreover, three transcripts of orf222 were detected in the floral buds of NCa cms and fertile F1, but no transcript was detected in floral buds of the maintainer line.The transcription of orf139 was similar to that of orf222 but only two transcripts of 0.8 kb and 0.6 kb were produced. The atp9 probe detected a single transcript of 0.6 kb in NCa cms and in maintainer line and an additional transcript of 1.2 kb in fertile F1. The relationship of expression of orf222, orf139, and atp9 with NCa sterility was discussed.
文摘程序化细胞死亡蛋白-1(programmed cell death protein-1, PD-1)是一个由Pdcd1编码的抑制性辅助受体(co-inhibitory receptor),它对T细胞的免疫应答具有重要的调节作用。PD-1信号通路在急性感染过程中可以防止T细胞的过度激活,但是在慢性感染过程中可以引起T细胞耗竭(T cell exhaustion)。肿瘤浸润T细胞(tumor-infiltrating T cells)高表达PD-1可以导致肿瘤细胞的免疫逃逸,靶向PD-1信号通路的免疫治疗已经在肿瘤治疗方面取得了巨大的成功。Pdcd1在免疫细胞中的表达存在复杂的调控机制,本文将对这方面的研究进展作一综述。