Death comes in small packages
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《细胞学杂志》
McKay/NAS
Killer sunburns are detected by the smallest of genes, according to Bruce McKay and colleagues (Ottawa Regional Cancer Centre, Ottawa, ON). A bias toward damage of larger genes leaves intact only the tiny genes, which make sure that overdamaged cells die.
UV rays create DNA lesions that block RNA polymerases. A little damage can be cleaned up by UV-induced repair pathways that remove the lesions. But too much UV—which may make more lesions than can be repaired—triggers apoptosis instead. McKay now shows that the small size of apoptotic genes means that they rule when UV levels are high.
The authors find that fewer genes are transcribed as UV levels increase, and those that are transcribed are smaller, with fewer and shorter introns. These small genes include many known mitochondrial apoptotic genes, which were activated at the highest UV dose tested. Genes encoding repair proteins or survival proteins, such as Bcl-XL, were induced only at low UV levels, probably because they are larger and more likely to suffer from transcription-blocking lesions.
"The shift in the pattern of gene expression is the result of a passive mechanism," says McKay. So no extra energy is needed to convince highly injured cells to die.
Reference:
McKay, B., et al. 2004. Proc. Natl. Acad. Sci. USA. 10.1073/pnas.0308181101.(The transcription of survival genes (whi)
娣団剝浼呮禒鍛返閸欏倽鈧喛绱濇稉宥嗙€幋鎰崲娴ｆ洑绠ｅ楦款唴閵嗕焦甯归懡鎰灗閹稿洤绱╅妴鍌涙瀮缁旂姷澧楅弶鍐ㄧ潣娴滃骸甯拋妞剧稊閺夊啩姹夐敍宀冨閹劏顓绘稉鐑橆劃閺傚洣绗夌€规粏顫﹂弨璺虹秿娓氭稑銇囩€硅泛鍘ょ拹褰掓鐠囦紮绱濈拠鐑藉仏娴犺埖鍨ㄩ悽浣冪樈闁氨鐓￠幋鎴滄粦閿涘本鍨滄禒顒佹暪閸掍即鈧氨鐓￠崥搴礉娴兼氨鐝涢崡鍐茬殺閹劎娈戞担婊冩惂娴犲孩婀扮純鎴犵彲閸掔娀娅庨妴锟�Killer sunburns are detected by the smallest of genes, according to Bruce McKay and colleagues (Ottawa Regional Cancer Centre, Ottawa, ON). A bias toward damage of larger genes leaves intact only the tiny genes, which make sure that overdamaged cells die.
UV rays create DNA lesions that block RNA polymerases. A little damage can be cleaned up by UV-induced repair pathways that remove the lesions. But too much UV—which may make more lesions than can be repaired—triggers apoptosis instead. McKay now shows that the small size of apoptotic genes means that they rule when UV levels are high.
The authors find that fewer genes are transcribed as UV levels increase, and those that are transcribed are smaller, with fewer and shorter introns. These small genes include many known mitochondrial apoptotic genes, which were activated at the highest UV dose tested. Genes encoding repair proteins or survival proteins, such as Bcl-XL, were induced only at low UV levels, probably because they are larger and more likely to suffer from transcription-blocking lesions.
"The shift in the pattern of gene expression is the result of a passive mechanism," says McKay. So no extra energy is needed to convince highly injured cells to die.
Reference:
McKay, B., et al. 2004. Proc. Natl. Acad. Sci. USA. 10.1073/pnas.0308181101.(The transcription of survival genes (whi)
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