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Telosma mosaic virus (TeMV) is a highly infectious and rapidly spreading virus that infects a variety of natural hosts, with passion fruit (Passiflora edulis) being its primary host across parts of Asia. Symptoms of TeMV, which seriously threatens passion fruit production worldwide, include mosaic, deformities and lignification of fruit. We present here a review of the current state of knowledge of TeMV, including its structural characteristics, natural and experimental host range, symptoms and detection, and provide insights into control strategies. The mode of transmission of TeMV remains unclear, but it can be mechanically transmitted through grafting, cuttings and other artificial asexual propagation techniques, which unfortunately constitute the primary means of propagation in the passion fruit industry. Moreover, increasing detection rates of TeMV indicate that this virus probably causes more serious losses to the passion fruit industry than previously reported. No systematic control strategy for TeMV infection currently exists, and no TeMV‐resistant passion fruit varieties are currently available. As a speedy, short‐term solution for dealing with TeMV infection in the absence of a long‐term solution, we propose rapid plant propagation through virus‐free plant tissue culture techniques that can generate a substantial number of virus‐free passion fruit seedlings. [ABSTRACT FROM AUTHOR]

• LRRK2 G2385R mutation is the most common mutation of LRRK2 in Asia, especially in the Chinese Han population. • LRRK2 G2385R mutation impairs mitochondrial function by affecting mitochondrial biogenesis. • Idebenone rescues mitochondrial dysfunction and cellular damage caused by LRRK2 G2385R mutation. Mutations in the Leucine-rich repeat protein kinase 2 (LRRK2) gene are the most frequent cause of familial Parkinson's disease (PD). Although LRRK2 has been extensively studied, the pathogenic mechanism of the LRRK2 G2385R mutation, which is most common in Asian populations, especially in the Chinese Han population, remains unclear. In this study, we demonstrated that the LRRK2 G2385R mutation in HEK293T cells led to a reduction in cellular PGC-1α protein expression and inhibition of mitochondrial biogenesis through the PGC-1α-TFAM pathway. This resulted in a decrease in mitochondrial genome expression, which in turn impaired the normal electron transfer process of the oxidative phosphorylation respiratory chain, leading to mitochondrial dysfunction and onset of apoptosis. The mitochondrial dysfunction and apoptosis caused by the LRRK2 G2385R mutation were significantly alleviated by antioxidant Idebenone, which provides a theoretical basis for the subsequent development of precise treatment specifically for PD patients with LRRK2 G2385R mutation. Further validation of our findings in neurons and animal models are necessary. [ABSTRACT FROM AUTHOR]