2010年2月19日的《细胞》（Cell）杂志刊载了清华大学生命科学学院钟毅教授在短期记忆遗忘机理研究方面取得的重大进展。刚刚获取的记忆通常会很快遗忘，该论文认为这样的快速遗忘其实是一种主动的行为，用以抹掉旧的记忆腾出空间来存储新的记忆，在果蝇中，小G蛋白Rac对主动遗忘具有调控作用。通过分子遗传方法操纵Rac的活性即可改变果蝇遗忘的速度，Rac活性低时，遗忘变慢，活性高时，遗忘加速。钟毅教授这篇题为“果蝇遗忘受小G蛋白Rac调控”("Forgetting Is Regulated through Rac Activity in Drosophila")的论文极大地挑战了人们把遗忘当成一个被动、负面过程的传统看法；因而被《细胞》杂志选为这一期的特色文章(Featured Article)，并得到诸多公众媒体如《纽约时报》、《科学美国人》的关注。
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《细胞》发表论文摘要（英文）
Cell, Volume 140, Issue 4, 579-589, 19 February 2010 . | 10.1016/j.cell.2009.12.044
Forgetting Is Regulated through Rac Activity in Drosophila
Highlights
Memory decay is bidirectionally regulated by genetic manipulation of Rac activity
Interference-induced forgetting is suppressed by Rac inhibition
Flexible behavior in reversal learning is altered by Rac activity manipulation
Endogenous Rac is activated in parallel with forgetting
Summary
Initially acquired memory dissipates rapidly if not consolidated. Such memory decay is thought to result either from the inherently labile nature of newly acquired memories or from interference by subsequently attained information. Here we report that a small G protein Rac-dependent forgetting mechanism contributes to both passive memory decay and interference-induced forgetting in Drosophila. Inhibition of Rac activity leads to slower decay of early memory, extending it from a few hours to more than one day, and to blockade of interference-induced forgetting. Conversely, elevated Rac activity in mushroom body neurons accelerates memory decay. This forgetting mechanism does not affect memory acquisition and is independent of Rutabaga adenylyl cyclase-mediated memory formation mechanisms. Endogenous Rac activation is evoked on different time scales during gradual memory loss in passive decay and during acute memory removal in reversal learning. We suggest that Rac's role in actin cytoskeleton remodeling may contribute to memory erasure.
