Fragile X syndrome (FXS), caused by a mutation in the Fragile X Mental Retardation 1 (FMR1) gene, is a common form of inherited mental retardation. Mutation of the gene leads to a loss of the gene product Fragile X Mental Retardation Protein (FMRP). While a loss of FMRP has been primarily associated with neural and cognitive deficits, it has also been reported to lead to immune system dysfunction in both humans and flies. We used the Acheta domesticus transcriptome to identify a highly conserved cricket ortholog of FMR1 (adfmr1). We cloned a partial cDNA of adfmr1, used systemic RNA interference (RNAi) to knockdown adfmr1 expression, and examined the impact of this knockdown (KD) on the cellular and humoral responses of the insect innate immune system. Following RNAi, both male and female crickets exhibited an increase in the number of circulating hemocytes, a decrease in total hemolymph phenoloxidase (PO) activity, and an increase in fat body lysozyme expression. Despite similar changes in these immune parameters in both sexes, male and female crickets responded differently to an immune challenge. Most KD males failed to survive an intra-abdominal injection of bacterial lipopolysaccharide, while KD females were just as likely as control females to survive this challenge. Our results support that decreased fmr1 expression can alter the cellular and humoral defenses of the insect innate immune system, and may lead to a decrease in male, but not female, immunocompetence.

由脆性X智力低下1（FMR1）基因突变引起的脆性X综合征（FXS）是遗传性智力低下的常见形式。基因突变导致基因产物脆性X智力低下蛋白（FMRP）丢失。尽管FMRP的丧失主要与神经和认知缺陷有关，但据报道它还导致人类和果蝇的免疫系统功能障碍。我们使用Acheta domesticus转录组来鉴定FMR1（adfmr1）的高度保守的or直系同源基因。我们克隆了adfmr1的部分cDNA ，使用系统性RNA干扰（RNAi）敲低adfmr1表达，并检查了这种击倒（KD）对昆虫先天免疫系统的细胞和体液反应的影响。继RNAi后，雄性和雌性both均表现出循环血细胞数量增加，总血淋巴酚氧化酶（PO）活性降低以及脂肪体溶菌酶表达增加。尽管这些免疫参数在男女中都有相似的变化，但男性和女性对免疫挑战的反应却不同。多数KD雄性在腹腔内注射细菌性脂多糖失败后存活下来，而KD雌性则与对照雌性一样幸免于这一挑战。我们的结果支持降低fmr1 表达可改变昆虫固有免疫系统的细胞和体液防御，并可能导致雄性而非雌性免疫能力降低。