c-myc腫瘍遺伝子のmRNAのレベルは,細胞サイクルを通して不変である

C B Thompson, P B Challoner, P E Neiman

Nature

|March 3, 1985

まとめ

プロトオンコゲンc-myc mRNAのレベルは,細胞サイクル中に変動しない. この発見は,c-mycの調節を,チミジンキナーゼやヒストン2bのような細胞周期に依存する遺伝子と区別する.

科学分野:

分子生物学は分子生物学である.
細胞生物学細胞生物学
遺伝子発現の表現について

背景:

プロトオンコゲンc-myc mRNAのレベルは,静止細胞の増殖を刺激すると一時的に上昇します.
この一時的な増加は,c-mycの発現が細胞周期のG1段階に特異的であるという仮説につながった.
別の仮説では,この増加は,細胞サイクルへの入り口を可能にする活性化イベントを反映していると考えられている.

研究の目的:

継続的に増殖する細胞の細胞サイクル中にc-myc mRNAレベルが変動するかどうかを判断する.
細胞周期特異的調節とc-myc.の活性化依存的発現を区別する.
c-myc mRNAの調節を他の増殖関連遺伝子と比較する.

主な方法:

細胞培養は,継続的な増殖刺激の下で行われます.
継続的に成長する細胞の細胞サイクル全体でc-myc mRNAレベルを測定する.
成長因子で維持された密度停止細胞のc-myc mRNAレベルを評価する.
c-myc mRNAのダイナミクスをチミジンキナーゼ (TK) とヒストン2b (H2b) mRNAレベルと比較する.

主要な成果:

c-myc mRNAレベルは,連続的に増殖する細胞の細胞サイクル全体で一定である.
c-myc mRNAレベルは,継続的な成長因子の存在下で,密度停止細胞では減少しません.
対照的に,TKとH2bのmRNAレベルは,細胞周期に依存する変化を示し,S段階では増加し,成長停止時に減少します.

結論:

静止細胞の活性化時に発生するc-myc mRNAの一時的な増加は,細胞周期特有の調節によるものではない.
c-mycの調節は,細胞サイクル進行と密接に関連しているTKとH2bの調節とは異なる.
c-myc発現のダイナミクスは,単純な細胞サイクルフェーズ特異性を超える役割を示唆しています.

さらに関連する動画

12:02

Studying Cell Cycle-regulated Gene Expression by Two Complementary Cell Synchronization Protocols

Published on: June 6, 2017

09:09

Preparation of Primary Acute Lymphoblastic Leukemia Cells in Different Cell Cycle Phases by Centrifugal Elutriation

Published on: November 10, 2017

関連する概念動画

01:45

Positive Regulator Molecules

To consistently produce healthy cells, the cell cycle—the process that generates daughter cells—must be precisely regulated.

02:39

Positive Regulator Molecules

Mitotic cell division results in daughter cells that exactly resemble the parent cell. However, errors in the DNA replication or distribution of genetic material may lead to genetic mutations that may be passed down to every new cell formed from the resulting abnormal cell. Propagation of such mutant cells is restricted through checkpoint mechanisms present at different stages of the cell cycle. These checkpoints involve regulator molecules that either promote or demote cell cycle events.

02:34

Inhibition of Cdk Activity

The orderly progression of the cell cycle depends on the activation of Cdk protein by binding to its cyclin partner. However, the cell cycle must be restricted when undergoing abnormal changes. Most cancers correlate to the deregulated cell cycle, and since Cdks are a central component of the cell cycle, Cdk inhibitors are extensively studied to develop anticancer agents. For instance, cyclin D associates with several Cdks, such as Cdk 4/6, to form an active complex. The cyclin D-Cdk4/6 complex...

02:15

M-Cdk Drives Transition Into Mitosis

Checkpoints throughout the cell cycle serve as safeguards and gatekeepers, allowing the cell cycle to progress in favorable conditions and slow or halt it in problematic ones. This regulation is known as the cell cycle control system.
Cyclin-dependent kinases, or Cdks, work in concert with cyclins to control cell cycle transitions. M-Cdk, a complex of Cdk1 bound to M cyclin, is a well-known example of this coordinated control that drives the transition from the G2 to the M phase.
M cyclin...

02:38

Mitogens and the Cell Cycle

Mitogens and their receptors play a crucial role in controlling the progression of the cell cycle. However, the loss of mitogenic control over cell division leads to tumor formation. Therefore, mitogens and mitogen receptors play an important role in cancer research. For instance, the epidermal growth factor (EGF) - a type of mitogen and its transmembrane receptor (EGFR), decides the fate of the cell's proliferation. When EGF binds to EGFR, a member of the ErbB family of tyrosine kinase...