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Mismatch Repair01:36

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Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the...
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Organisms are capable of detecting and fixing nucleotide mismatches that occur during DNA replication. This sophisticated process requires identifying the new strand and replacing the erroneous bases with correct nucleotides. Mismatch repair is coordinated by many proteins in both prokaryotes and eukaryotes.
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MBNLタンパク質は,ES細胞特異的な代替スプライシングと再プログラミングを抑制する.

Hong Han1, Manuel Irimia, P Joel Ross

  • 1Banting and Best Department of Medical Research and Donnelly Centre, University of Toronto, Toronto, Ontario M5S 3E1, Canada.

Nature
|June 7, 2013
PubMed
まとめ

筋肉盲のような (MBNL) タンパク質は,代替スプライシングを制御することによって,胚性幹細胞 (ES) の多能性を調節する. それらの欠如は,多能性遺伝子発現と再プログラムを促進し,新しい規制メカニズムを明らかにします.

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科学分野:

  • 分子生物学は分子生物学である.
  • 発達生物学 発達生物学について
  • 遺伝子規制 遺伝子規制

背景:

  • 胚性幹細胞 (ES) の多能性は,主に転写,クロマチン,および非コーディングRNAを通じて研究されています.
  • ES細胞の多能性と分化における代替スプライシングの役割は,依然としてほとんど未調査のままである.

研究 の 目的:

  • ES細胞の多能性と微分化の調節における代替スプライシングの役割を調査する.
  • ES細胞における代替スプライシングの重要なレギュレータを特定する.

主な方法:

  • 代替スプライシングのレギュレーターとして,筋肉盲のような (MBNL) タンパク質 (MBNL1とMBNL2) を特定した.
  • 差別化された細胞におけるMBNLタンパク質のノックダウンと,ES細胞における過剰発現が,代替スプライシングパターンに与える影響を調査した.
  • FOXP1転写因子を含む MBNL 調節された代替スプライシングイベントを分析した.

主要な成果:

  • MBNL1とMBNL2は,ES細胞におけるカセットエクソン代替スプライシングの直接的負の調節体である.
  • 微分細胞におけるMBNLのノックダウンは,ES細胞のようなスプライシングパターンを誘発し,ES細胞におけるMBNLの過剰発現は,微分細胞のようなスプライシングを促進した.
  • MBNLタンパク質は,多能性を制御する転写因子であるFOXP1のES細胞特異的な代替スプライシングスイッチを調節する.
  • MBNLのノックダウンにより,再プログラム中に多能性遺伝子発現が強化され,多能性幹細胞の形成が誘発された.

結論:

  • MBNLタンパク質は,代替スプライシングを通じて,ES細胞の多能性を維持する中心的な,負の調節的な役割を果たします.
  • MBNLタンパク質によって調節される代替スプライシングは,ES細胞の多能性および体細胞再プログラムにおける重要なメカニズムです.