The phytohormone auxin has been known for >50 years to be required for entry into the cell cycle. Despite the critical effects exerted by auxin on the control of cell division, the molecular mechanism by which auxin controls this pathway is poorly understood, and how auxin is perceived upstream of any change in the cell cycle is unknown. Auxin Binding Protein 1 (ABP1) is considered to be a candidate auxin receptor, triggering early modification of ion fluxes across the plasma membrane in response to auxin. ABP1 has also been proposed to mediate auxin-dependent cell expansion, and is essential for early embryonic development. We investigated whether ABP1 has a role in the cell cycle. Functional inactivation of ABP1 in the model plant cell system BY2 was achieved through cellular immunization via the conditional expression of a single-chain fragment variable (scFv). This scFv was derived from a well characterized anti-ABP1 monoclonal antibody previously shown to block the activity of the protein. We demonstrate that functional inactivation of ABP1 results in cell-cycle arrest, and provide evidence that ABP1 plays a critical role in regulation of the cell cycle by acting at both the G1/S and G2/M checkpoints. We conclude that ABP1 is essential for the auxin control of cell division and is likely to constitute the first step of the auxin-signalling pathway mediating auxin effects on the cell cycle.
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http://dx.doi.org/10.1111/j.1365-313X.2007.03038.x | DOI Listing |
BMC Cancer
January 2025
Department of Biochemistry, School of Medicine, Iran University of Medical Sciences, Tehran, Iran.
Background: Inadequate treatment responses, chemotherapy resistance, significant heterogeneity, and lengthy treatment durations create an urgent need for new pancreatic cancer therapies. This study aims to investigate the effectiveness of gemcitabine-loaded nanoparticles enclosed in an organo-metallic framework under ketogenic conditions in inhibiting the growth of MIA-PaCa-2 cells.
Methods: Gemcitabine was encapsulated in Metal-organic frameworks (MOFs) and its morphology and size distribution were examined using transmission electron microscopy (TEM) and Dynamic light scattering (DLS) with further characterization including FTIR analysis.
Hum Cell
January 2025
Department of Nephrology, Zhong Da Hospital, Gulou District, No. 87, Dingjiaqiao, Zhongyangmen Street, Nanjing, 210009, Jiangsu, China.
Autophagy, a cellular degradation process involving the formation and clearance of autophagosomes, is mediated by autophagic proteins, such as microtubule-associated protein 1 light chain 3 (LC3) and sequestosome 1 (p62), and modulated by 3-methyladenine (3-MA) as well as chloroquine (CQ). Senescence, characterised by permanent cell cycle arrest, is marked by proteins such as cyclin-dependent kinase inhibitor 1 (p21) and tumour protein 53 (p53). This study aims to investigate the relationship between cell senescence and renal function in diabetic kidney disease (DKD) and the effect of autophagy on high-glucose-induced cell senescence.
View Article and Find Full Text PDFNat Cell Biol
January 2025
Department of Molecular, Cell and Developmental Biology, University of California, Los Angeles, Los Angeles, CA, USA.
Many of the cells in mammalian tissues are in a reversible quiescent state; they are not dividing, but retain the ability to proliferate in response to extracellular signals. Quiescence relies on the activities of transcription factors (TFs) that orchestrate the repression of genes that promote proliferation and establish a quiescence-specific gene expression program. Here we discuss how the coordinated activities of TFs in different quiescent stem cells and differentiated cells maintain reversible cell cycle arrest and establish cell-protective signalling pathways.
View Article and Find Full Text PDFNat Cell Biol
January 2025
Department of Biochemistry, University of Oxford, Oxford, UK.
Delays in mitosis trigger p53-dependent arrest in G1 of the next cell cycle, thus preventing repeated cycles of chromosome instability and aneuploidy. Here we show that MDM2, the p53 ubiquitin ligase, is a key component of the timer mechanism triggering G1 arrest in response to prolonged mitosis. This timer function arises due to the attenuation of protein synthesis in mitosis.
View Article and Find Full Text PDFNat Struct Mol Biol
January 2025
Key Laboratory of Biomacromolecules (CAS), National Laboratory of Biomacromolecules, CAS Center for Excellence in Biomacromolecules, Institute of Biophysics, Chinese Academy of Sciences, Beijing, China.
Many protein complexes are highly dynamic in cells; thus, characterizing their conformational changes in cells is crucial for unraveling their functions. Here, using cryo-electron microscopy, 451,700 ribosome particles from Saccharomyces cerevisiae cell lamellae were obtained to solve the 60S region to 2.9-Å resolution by in situ single-particle analysis.
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