果蝇长时程记忆缺陷型突变体的鉴定

长时程记忆作为依赖蛋白合成的记忆组分，对于了解高等认知活动的分子机制有着重要意义.与此同时，细胞粘连分子作为影响突触可塑性的重要因子在学习与记忆研究领域也日益得到重视.为探索作用于长时程记忆的细胞粘连分子，利用P因子在果蝇基因组随机插入制造突变体，并通过大规模行为筛选得到了一个可能的长时程记忆突变体RUO. 测序结果表明，突变体RUO的P因子位于果蝇中selectin超家族对应的furrowed同源基因功能片段和未知功能的CG1806基因编码片段之间，且更靠近furrowed片段.RT-PCR结果和互补遗传学实验均表明,突变体RUO主要影响furrowed基因的表达.为了进一步确认furrowed基因与长时程记忆的相关性，引入已知的furrowed基因突变体fw1.结果表明，fw1同样具有长时程记忆缺陷，同时具备正常的学习能力.荧光共聚焦扫描成像显示，该基因特异性的表达在果蝇大脑两个对称的未知神经元中.此项工作不仅证明了furrowed基因在果蝇长时程记忆中的重要作用，而且在解剖学上揭示了果蝇神经系统中可能参与长时程记忆形成的新的神经元.

Identifying Furrowed Mutant in Drosophila with Long-term Memory Deficience

Long-term memory related protein synthesis is a significant aspect for understanding of advanced cognitive behavior. Exploration of the relationship between long-term memory and adhesion molecules helped to link synaptic plasticity change with behavior modification. To discover novel adhesion molecules participating memory formation, we screened for defective long-term memory mutants in Drosophila of P-element inserted stocks, and obtained one defective mutant RUO. DNA sequencing and RT-PCR showed that the P-element in RUO mutant only disrupted the expression of the protein furrowed, an adhesion molecule of selectin superfamily. Both RUO mutant and an existed furrow mutant fw1 were observed defective for long-term memory in behavior experiments, but with normal aversive learning abilities. The genetic complementation test showed that RUO/fw1 was also defective for 24-hours memory. The furrowed expression was only found in the two symmetric neurons, which were excluded from the known long-term memory neural circuitry. Our results implied that furrowed was an adhesion molecule decisive in cognitive behavior and resided in neurons responsible for the memory formation and storage process.