Exploring the Mystery of the Tetrahydrobiopterin Synthetic Defect Lethal Mutant lem(l) from Birth to Death in the Silkworm Bombyx mori
文献类型： 外文期刊
作者： Liang, Dan 1 ; Shu, Rui 1 ; Jiang, Song 1 ; Xu, Mengjun 1 ; Cai, Yangyang 1 ; Qin, Hongwei 1 ; Zhang, Daobo 1 ; Feng, Mengwei 1 ; Gao, Junshan 1 ; Meng, Yan 1 ;
作者机构： 1.Anhui Agr Univ, Sch Life Sci, 130 West Changjiang Rd, Hefei 230036, Peoples R China
2.Anhui Acad Agr Sci, Inst Sericulture, 15 Huoshan Rd, Hefei 230061, Peoples R China
3.Anhui Int Joint Res & Dev Ctr Sericulture Resourc, Hefei 230036, Peoples R China
关键词： maternal effect; mitochondrial damage; immune system; apoptosis system; oxidative stress
期刊名称：INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES （ 影响因子：6.208； 五年影响因子：6.628 ）
ISSN：
年卷期： 2022 年 23 卷 20 期
页码：
收录情况： SCI
摘要： Tetrahydrobiopterin (BH4) is a vital coenzyme for several enzymes involved in diverse enzymatic reactions in animals, and BH4 deficiency can lead to metabolic and neurological disorders due to dysfunction in its metabolism. In the silkworm natural homozygous mutant lem(l), the key enzyme sepiapterin reductase (BmSPR) in the de novo synthesis pathway of BH4 is inactivated, resulting in severe deficiency of BH4 synthesis. However, it is not known why the lem(l) larvae can survive to the second-instar stage and which pathways lead to their death when BH4 is deficient. Here, we quantified BH4 and found that the fertilized eggs contained large amounts of BH4 transferred from the mother to the offspring, maintaining its normal development in the embryo and the first instar. Subsequently, we investigated the multiple pathways in which BH4 is involved as a cofactor. The results showed that BH4 deficiency in silkworms blocked the melanin synthesis pathway, caused an insufficient degree of epidermal sclerosis, disordered tyrosine metabolism, and damaged mitochondria. On the other hand, BH4 deficiency led to the uncoupling of nitric oxide synthase (BmNOS), a reduced NO production, and a significantly reduced fat in fat body catalyzation by phospholipase A2, resulting in an impaired immune system. Meanwhile, the uncoupling of BmNOS increased the O-2(-) content, damaged the DNA, and caused the apoptosis of the body cells. Taken together, BH4 is critical for the life and death of lem(l) mutants. This study lays a foundation for the further exploration of lepidopteran insects and provides an important basis for the treatment of human BH4 deficiency-related diseases.
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