2つのプロモーターからSV40早期転写のT抗原抑制

U Hansen¹, D G Tenen, D M Livingston

¹Center for Cancer Research, Massachusetts Institute of Technology, Cambridge 02139.

Cell

|December 1, 1981

まとめ

SV40初期のmRNAは腫瘍抗原をコードする. T抗原アナログであるD2Tは,特定の部位での転写開始を抑制し,リティックサイクル中のmRNA処理に影響を与えます.

科学分野:

分子生物学は分子生物学である.
ウイルス学ウイルス学ウイルス学

背景:

シミアンウイルス40 (SV40) の初期のmRNAは,大きな腫瘍抗原 (T) と小さな腫瘍抗原 (t) をコードする.
SV40リティックサイクルでは,5'mRNA端末のシフトが起こり,転写開始部位が変化します.

研究の目的:

転写開始部位の選択とSV40T抗原による抑制のメカニズムを調査する.
初期のmRNA処理の調節におけるT抗原結合の役割を明らかにする.

主な方法:

SV40早期mRNA開始部位を用いたインビトロ転写アッセイ.
異なる濃度でのT抗原アナログ (D2T) による転写抑制の分析.

主要な成果:

アップストリームとダウンストリームの両方のイニシアチブサイトは,in vitroで利用されます.
D2Tは,両方の部位からの転写を抑制し,濃度に依存した明確な効果をもたらします.
D2Tを特定のサイト (I,II) に縛ることは,それぞれ下流および上流のイニシアチブを抑制することと相関しています.

結論:

SV40 T抗原は,転写開始部位の使用を調節する上で重要な役割を果たします.
調節部位へのT抗原の差異結合は,リティックサイクル中のmRNA処理のシフトを制御する.

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