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Mitochondria change their morphology in response to developmental and environmental cues. During sexual reproduction, bryophytes produce spermatozoids with two mitochondria in the cell body. Although intensive morphological analyses have been conducted, how this fixed number of mitochondria is realized remains poorly understood. Here, we investigate how mitochondria are reorganized during spermiogenesis in Marchantia polymorpha. We find that the mitochondrial number is reduced to one through fission followed by autophagic degradation during early spermiogenesis, and then the posterior mitochondrion arises by fission of the anterior mitochondrion. Autophagy is also responsible for the removal of other organelles, including peroxisomes, but these other organelles are removed at distinct developmental stages from mitochondrial degradation. We also find that spermiogenesis involves nonautophagic organelle degradation. Our findings highlight the dynamic reorganization of mitochondria, which is regulated distinctly from that of other organelles, and multiple degradation mechanisms operate in organelle remodeling during spermiogenesis in M. polymorpha.
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http://dx.doi.org/10.1016/j.celrep.2022.110975 | DOI Listing |
Fungal Biol
October 2025
Institute of Food Bioscience and Technology, College of Biosystems Engineering and Food Science, Zhejiang University, Hangzhou, 310058, Zhejiang, China. Electronic address:
Penicillium expansum is a phytopathogen causing postharvest disease of many fruits, which has led to enormous losses. Therefore, it is of great significance to take efficient methods to control this notorious phytopathogen. In this study, zinc, an essential trace element for human body, has been found to be able to effectively inhibit the P.
View Article and Find Full Text PDFMicrobes Infect
September 2025
Department of Pulmonary and Critical Care Medicine, The Second Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi 530007, P.R. China. Electronic address:
Background: While autophagy is pivotal in antimicrobial defense, its regulatory role in Talaromyces marneffei (TM) infected bronchial epithelium remains elusive.
Objective: To elucidate the impact of TM infection on autophagy in bronchial epithelial cells and to identify the key molecular regulators involved in this process.
Methods: Primary computational screening identified core autophagy modulators.
Chem Biol Interact
September 2025
Department of Human Development and Family Studies, National Taiwan Normal University, Taipei 10610, Taiwan; Nutrition Science, School of Life Science, National Taiwan Normal University, Taipei 11677, Taiwan. Electronic address:
Accumulated dysfunctional mitochondria are involved in tumorigenesis, and it is conceivable that mitophagy, a selective form of autophagic degradation of mitochondria, plays a tumor-suppressive role. Our bioinformatics analysis identified lignan justicidin A (JA) as a potential mitophagy inducer. In HRAS-mutant human bladder cancer T24 cells, JA reduced population cell growth, changed mitochondrial membrane potential, and induced autophagy.
View Article and Find Full Text PDFBiomater Sci
September 2025
School of Medical Technology, Beijing Institute of Technology, Beijing 100081, China.
Cancer immunotherapy has transformed oncological treatment paradigms, yet tumor resistance and immune evasion continue to limit therapeutic efficacy. Mitochondria-targeting organic sensitizers (MTOSs) represent an emerging class of therapeutic agents that exploit mitochondrial dysfunction as a convergent node for tumor elimination and immune activation. As central regulators of cellular metabolism, apoptotic signaling, and immune cell function, mitochondria serve as critical determinants of tumor progression and the immunological landscape within the tumor microenvironment (TME).
View Article and Find Full Text PDFAdv Sci (Weinh)
September 2025
Second Division of Department of Oncology, China-Japan Union Hospital of Jilin University, Changchun, Jilin, 130031, China.
Ferroptosis, characterized by iron-dependent lipid peroxidation, is a form of oxidative cell death increasingly recognized for its role in cancer therapy. The susceptibility of cancer cells to ferroptosis varies, highlighting the need to elucidate its underlying metabolic mechanisms. This study identifies a novel pathway in which the E3 ubiquitin ligase, praja ring finger ubiquitin ligase 1 (PJA1), mediates the proteasomal degradation of glyoxalase I (GLO1) exclusively in ferroptosis-sensitive cancer cells.
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