The Golgi apparatus is the central hub of intracellular trafficking and consists of tethered stacks of cis, medial, and trans cisternae. In mammalian cells, these cisternae are stitched together as a perinuclear Golgi ribbon, which is required for the establishment of cell polarity and normal subcellular organization. We previously identified FHDC1 (also known as INF1) as a unique microtubule-binding member of the formin family of cytoskeletal-remodeling proteins. We show here that endogenous FHDC1 regulates Golgi ribbon formation and has an apparent preferential association with the Golgi-derived microtubule network. Knockdown of FHDC1 expression results in defective Golgi assembly and suggests a role for FHDC1 in maintenance of the Golgi-derived microtubule network. Similarly, overexpression of FHDC1 induces dispersion of the Golgi ribbon into functional ministacks. This effect is independent of centrosome-derived microtubules and instead likely requires the interaction between the FHDC1 microtubule-binding domain and the Golgi-derived microtubule network. These effects also depend on the interaction between the FHDC1 FH2 domain and the actin cytoskeleton. Thus our results suggest that the coordination of actin and microtubule dynamics by FHDC1 is required for normal Golgi ribbon formation.
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http://dx.doi.org/10.1091/mbc.E15-02-0070 | DOI Listing |
Nat Commun
December 2024
Shenzhen Institute of Synthetic Biology, Shenzhen Institutes of Advanced Technology, Chinese Academy of Sciences, Shenzhen, 518055, China.
Iron is a potent biochemical, and accurate homeostatic control is orchestrated by a network of interacting players at multiple levels. Although our understanding of organismal iron homeostasis has advanced, intracellular iron homeostasis is poorly understood, including coordination between organelles and iron export into the ER/Golgi. Here, we show that SLC39A13 (ZIP13), previously identified as a zinc transporter, promotes intracellular iron transport and reduces intracellular iron levels.
View Article and Find Full Text PDFGenes Dev
December 2024
Howard Hughes Medical Institute, Department of Biological Sciences, Columbia University, New York, New York 10025, USA.
The pan-neuronally expressed and phylogenetically conserved CUT homeobox gene orchestrates pan-neuronal gene expression throughout the nervous system of As in many other species, including humans, is encoded by a complex locus that also codes for a Golgi-localized protein, called CASP (Cux1 alternatively spliced product) in humans and CONE-1 ("CASP of nematodes") in How gene expression from this complex locus is controlled-and, in , directed to all cells of the nervous system-has not been investigated. We show here that pan-neuronal expression of CEH-44/CUX is controlled by a pan-neuronal RNA splicing factor, UNC-75, the homolog of vertebrate CELF proteins. During embryogenesis, the locus exclusively produces the Golgi-localized CONE-1/CASP protein in all tissues, but upon the onset of postmitotic terminal differentiation of neurons, UNC-75/CELF induces the production of the alternative CEH-44/CUX CUT homeobox gene-encoding transcript exclusively in the nervous system.
View Article and Find Full Text PDFJ Microbiol Biotechnol
December 2024
Interdisciplinary Graduate Program in Advanced Convergence Technology & Science, Jeju National University, Jeju 63243, Republic of Korea.
Antiviral agents that target the viral envelope surface glycoproteins can disrupt the interactions between the viral glycoproteins and host cell receptors, thereby preventing viral entry into host cells. However, the mechanisms underlying glycoprotein processing and cellular trafficking have not been fully elucidated. In this study, we aimed to investigate the mechanism of action of cryptotanshinone (CTN) and dihydrotanshinone I (DTN) as inhibitors of viral glycoprotein trafficking, by assessing their inhibitory action on syncytium formation and cytopathic effects.
View Article and Find Full Text PDFTransl Neurodegener
December 2024
Department of Neurosciences, Hengyang Medical School, University of South China, Hengyang, 421009, China.
Background: Neurological complications are a significant concern of Coronavirus Disease 2019 (COVID-19). However, the pathogenic mechanism of neurological symptoms associated with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection is poorly understood.
Methods: We used Drosophila as a model to systematically analyze SARS-CoV-2 genes encoding structural and accessory proteins and identified the membrane protein (M) that disrupted mitochondrial functions in vivo.
Cell Mol Life Sci
December 2024
Department of Microbiology, Immunology and Infectious Diseases, University of Calgary, Calgary, AB, Canada.
Varicella-zoster virus (VZV) infection downregulates surface major histocompatibility complex class I (MHC-I) expression and retains MHC-I in the Golgi complex of infected cells. However, the underlying mechanism is not fully understood. The VZV IE4 protein is a multifunctional protein that is essential for VZV infection.
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