小鼠肌型磷酸果糖激酶基因内含子10和11的序列分析,特别参考外显子跳变。

Tomoyuki Yamasaki, Hiromu Nakajima, Tomoya Hamaguchi, Koji Tomita, Norio Kono, Kazuya Yamada, Tamio Noguchi
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摘要

为了阐明肌肉型磷酸果糖激酶(PFK-M)转录本11外显子跳变的生理相关性,我们对小鼠PFK-M的cDNA和基因组片段进行了部分克隆和分析。在RT-PCR分析中,使用一对携带人类11号外显子对应区域的引物,没有检测到任何不含11号外显子的次要转录物。对小鼠PFK-M基因进行部分测序分析,发现人基因的内含子10与小鼠基因的一致序列不一致,而人基因的内含子11与小鼠基因的一致序列无明显差异。这些结果表明,PFK-M基因转录本中外显子11的跳变主要存在于人体内。虽然需要进一步的研究来了解外显子跳变的机制和生理意义,但PFK-M转录本中的外显子跳变不太可能具有生理意义。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Sequence analysis of mouse muscle-type phosphofructokinase gene introns 10 and 11 with special reference to the exon skipping.

To elucidate physiological relevance of the skipping of exon 11 in muscle-type phosphofructokinase (PFK-M) transcripts, we partially cloned and analyzed the cDNA and the genomic fragment of mouse PFK-M. In RT-PCR analysis using a pair of primers which carry the region corresponding to human exon 11 in between, any minor transcript without exon 11 was not detected. Partial sequencing analysis of mouse PFK-M gene revealed that the junctions of intron 10 of human gene were both less identical to the consensus sequences than those of mouse gene, but that there was no appreciable difference in the junctions in intron 11 between mouse and human. These results suggest that the skipping of exon 11 in PFK-M gene transcripts would be found mainly in human. Although further investigation would be required to understand the mechanisms and physiological significance of exon-skipping, the exon-skipping in PFK-M transcripts would be unlikely to have the physiological significance.

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