关键词: Apoptosis Autophagy Degeneration Silk gland Transgenic silkworms

Mesh : Animals Bombyx / genetics Apoptosis / genetics Autophagy / genetics Silk / metabolism Animals, Genetically Modified Fibroins / genetics metabolism Larva / metabolism TOR Serine-Threonine Kinases / metabolism Insect Proteins / genetics metabolism

来  源:   DOI:10.1016/j.ijbiomac.2024.134312

Abstract:
The silkworm is an incredibly valuable insect that produces silk through its silk gland. Within this organ, Fibroinase has been identified and named due to its ability to fibroin degradation. The expression of Fibroinase in the silk gland significantly increases during the larval-pupal stage, which might be associated with the degeneration of the silk gland. In this study, Fibroinase was overexpressed and knocked down specifically both in the middle and posterior silk glands, respectively, using transgenic technology. The investigation of silk gland development in these transgenic silkworms showed that Fibroinase plays a direct role in accelerating silk gland degeneration. The staining analyses performed in the silk glands of transgenic silkworms suggest that Fibroinase is involved in the processes of autophagy and apoptosis during silk gland degeneration. Further experiments demonstrated that Fibroinase, acting as a lysosomal regulator, negatively regulates autophagy via the mTOR (mechanistic target of rapamycin) pathway. Moreover, during apoptosis, Fibroinase could activate Caspase3 by increasing the activity of BmCaspase1, ultimately accelerating the apoptosis process. These findings enhance our understanding of the physiological role of Fibroinase in promoting silk gland degeneration, which plays a role in breaking down proteins in the silk gland and coordinating the regulation of autophagy and apoptosis.
摘要:
蚕是一种非常有价值的昆虫,通过它的丝腺产生丝绸。在这个器官中,由于其能够降解丝心蛋白,因此已鉴定并命名了丝素酶。丝腺中丝素酶的表达在幼虫-p期显着增加,这可能与丝腺的退化有关。在这项研究中,纤维蛋白酶在中部和后部的丝腺中都被过表达并被特别地击倒。分别,使用转基因技术。对这些转基因蚕的丝腺发育的研究表明,纤维蛋白酶在加速丝腺变性中起直接作用。在转基因蚕的丝腺中进行的染色分析表明,纤维蛋白酶参与了丝腺变性过程中的自噬和凋亡过程。进一步的实验表明,纤维蛋白酶,作为溶酶体调节剂,通过mTOR(雷帕霉素的机制靶标)途径负调节自噬。此外,在细胞凋亡期间,纤维蛋白酶可以通过增加BmCaspase1的活性来激活Caspase3,最终加速细胞凋亡过程。这些发现增强了我们对纤维蛋白酶在促进丝腺变性中的生理作用的理解,丝腺中的蛋白质分解,协调自噬和凋亡的调节。
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