Role of Atg3, Atg5 and Atg12 in the crosstalk between apoptosis and autophagy in the posterior silk gland of Bombyx mori.

Abstract

Autophagy is a cellular mechanism that enhances cell survival in response to various stressors, including nutrient deprivation; however, it also plays a pivotal role in the regulation of programmed cell death. This study examined the effects of autophagy-related genes Atg3, Atg5 and Atg12 on apoptosis and autophagy during the degeneration of the posterior silk gland in Bombyx mori, employing RNA interference techniques. Apoptosis-specific markers and autophagic processes were evaluated in both control and treatment groups. The knockdown of all three genes resulted in a significant reduction in autophagy, modifications in the apoptosis process, aberrant expression of p53 and impaired lysosomal function. It was determined that Atg3 is involved in the regulation of intracellular mitochondrial homeostasis. Following the silencing of Atg5, evidence was obtained indicating the gene's role in regulating lysosomal pH. Notably, the loss of Atg3 and Atg5 was associated with an increase in apoptotic markers, whereas the silencing of Atg12 inhibited apoptosis. Elevated levels of the p53 transcription factor following gene silencing suggested a potential interaction between these genes and p53. Our findings further underscore the importance of autophagy-mediated cell death, involving Atg3, Atg5 and Atg12, in the proper progression of degeneration in the posterior silk gland. A comprehensive understanding of the molecular mechanisms that mediate the interaction between apoptosis and autophagy is essential for elucidating their roles in both physiological and pathological contexts.