マルチタスク遺伝子のおかげで人間のタンパク質の展開のスピードは緩やか Human Proteins Evolving Slowly Thanks To Multi-Tasking GenesThis is a featured page

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Human Proteins Evolving Slowly Thanks To Multi-Tasking Genes
Main Category: Biology / Biochemistry News
Article Date: 07 Feb 2007 - 14:00 PST
人間のタンパク質の多くは、本来の機能と比較してそれほど有効に機能しないが、それはそれを生成する遺伝子配列が二重の役割を持ち、このことで、展開のスピードが遅いとの研究報告。
この二重の役割の領域を引っ張ることで、自然な状態で生成されるものより良好なタンパク質を生成して遺伝子療法を開発できた。
特定のタンパク質を生成するDNAの広がりが、しばしば、明らかに無用なDNA、すなわちintronsといわれる部分で中断されており、新たなタンパク質生成のためには、改めて編集の必要がある。
最近、DNAをどの場所で切り離し、再度接続するかの命令の一部が、DNAそれ自身のプロブラム部分すなわちexon内に内蔵されていることが明らかになった。
従って,どのアミノ酸が特定のタンパク質製造のために必要かを定義するspell outと共に、intronに隣接するexonの部分が遺伝子編集プロセスに必須の情報を保有している。
このことは、仮に展開のプロセスが時間の経過とともにより改善されていたものと比較してこれらの遺伝子の部位は特に緩やかに進化し、本来生成されるものと比較すると性能が低い結果となる。
研究の結果、以下のことが想定できると研究者はいう。すなわち、多くのexonを有する遺伝子はintronを持たない同一の遺伝子と比較して半分のスピードで展開すると。その原因は単に、どの場所でinstronを除去するかを定義する必要があるためであると。
これは、これまでに知られている蛋白展開スピードの最強の予言者predictorであって、この二重のプログラム機能が従来考えられていたものと比較して、遥かに大きな影響を有することを示していると。
この研究成果は医薬品や欠陥遺伝子を持つ患者が正しいバージョンを投与される遺伝子療法技術の展開に大きな意味を持つと思われる。
この研究で、正常のバージョンより良い代替遺伝子を作成することができるだろうという。
何百万年も前にintronを喪失した遺伝子は、かつてintronが存在した周辺で特別に早く展開することも明らかになったという。
Many human proteins are not as good as they might be because the gene sequences that code for them have a double role which slows down the rate at which they evolve, according to new research published in PLoS Biology.

By tweaking these dual role regions, scientists could develop gene therapy techniques that produce proteins that are even better than those found in nature, and could one day be used to help people recover from genetic disorders.

The stretch of DNA which codes for a specific protein is often interrupted by sections of apparently useless DNA - known as introns - which need to be edited out in order to produce a new protein.

Recently it has been discovered that some of the instructions on where to splice and re-splice the DNA in this editing process are contained in the coding section, or exon, of the DNA itself.

So, as well as spelling out which amino acids are needed to produce a specific protein, the part of the exon immediately next to the intron contains information that is essential for the gene editing process.

This means that these parts of genes evolve particularly slowly, making the proteins they encode for not as good as they could be had evolutionary processes been more able to improve them over time.

"Our research suggests that a gene with many exons would evolve at under half the rate of the same one that had no introns, simply owing to the need to specify where to remove introns," said Professor Laurence Hurst from the University of Bath (UK), who worked with colleagues from the University of Lausanne (Switzerland) on the project.
"This is one of the strongest predictors of rates of protein evolution known, indicating that this dual coding role is vastly more influential than previously believed."
The finding could have major implications for medicine and the development of gene therapy techniques in which people with a defective gene are given the correct version.

"Our results suggest that we could make the replacement gene even better than the normal version," said Professor Hurst, from the Department of Biology & Biochemistry at the University of Bath.

"We would just need to remove the introns and tweak the protein at the sites that were dual coding.

"We also found that genes that have lost their introns many millions of years ago evolve especially fast near where the introns once resided.

"This indicates that this tweaking of the dual role sections of genes is also what evolution does when introns are removed."



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