Arabidopsis (Arabidopsis thaliana) trichome development is a model system for studying cell development, cell differentiation, and the cell cycle. Our previous studies have shown that the GLABROUS INFLORESCENCE STEMS (GIS) family genes, GIS, GIS2, and ZINC FINGER PROTEIN8 (ZFP8), control shoot maturation and epidermal cell fate by integrating gibberellins (GAs) and cytokinin signaling in Arabidopsis. Here, we show that a new C2H2 zinc finger protein, ZFP5, plays an important role in controlling trichome cell development through GA signaling. Overexpression of ZFP5 results in the formation of ectopic trichomes on carpels and other inflorescence organs. zfp5 loss-of-function mutants exhibit a reduced number of trichomes on sepals, cauline leaves, paraclades, and main inflorescence stems in comparison with wild-type plants. More importantly, it is found that ZFP5 mediates the regulation of trichome initiation by GAs. These results are consistent with ZFP5 expression patterns and the regional influence of GA on trichome initiation. The molecular analyses suggest that ZFP5 functions upstream of GIS, GIS2, ZFP8, and the key trichome initiation regulators GLABROUS1 (GL1) and GL3. Using a steroid-inducible activation of ZFP5 and chromatin immunoprecipitation experiments, we further demonstrate that ZFP8 is the direct target of ZFP5 in controlling epidermal cell differentiation.
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http://dx.doi.org/10.1104/pp.111.180281 | DOI Listing |
NAR Cancer
March 2025
Ribosome, Translation and Cancer Team, LaEx DEVweCAN, Institut Convergence Plascan, LYriCAN+, Centre de Recherche en Cancérologie de Lyon, INSERM U1052, CNRS UMR 5286, Centre Léon Bérard, Université de Lyon, Université Claude Bernard Lyon 1, 69008 Lyon, France.
The epithelial-mesenchymal transition (EMT) is a dynamic transdifferentiation of epithelial cells into mesenchymal cells. EMT programs exhibit great diversity, based primarily on the distinct impact of molecular activities of the EMT transcription factors. Using a panel of cancer cell lines and a series of 71 triple-negative primary breast tumors, we report that the EMT transcription factor ZEB1 modulates site-specific chemical modifications of ribosomal RNA (rRNA).
View Article and Find Full Text PDFCell Div
January 2025
Department of Nuclear Medicine, The Affiliated Cancer Hospital of Xiangya School of Medicine, Central South university/Hunan Cancer Hospital, No. 283 Tongzipo Road, Yuelu District, Changsha, 410013, Hunan, P.R. China.
Background: Zinc finger protein 169 (ZNF169) plays a key role in cancer development. However, the specific role of ZNF169 in the tumorigenesis of thyroid carcinoma (THCA) remains poorly understood.
Methods: The expression of ZNF169 was measured using immunohistochemistry, RT-qPCR, and western blot.
Plant Signal Behav
December 2025
Laboratory of Biotechnology and Natural Resources Valorization, Faculty of Sciences, Ibn Zohr University, Agadir, Morocco.
Various metabolic and cell signaling processes impact the functions of sugarcane plant cells. MicroRNAs (miRNAs) play critical regulatory roles in enhancing yield and providing protection against various stressors. This study seeks to identify and partially characterize several novel miRNAs in sugarcane using tools, while also offering a preliminary assessment of their functions.
View Article and Find Full Text PDFDiscov Oncol
January 2025
Department of Otolaryngology-Head and Neck Surgery, Nanfang Hospital, Southern Medical University, Guangzhou, 510515, China.
The zinc finger protein 32 (ZNF32) has been associated with high expression in various cancers, underscoring its significant function in both cancer biology and immune response. To further elucidate the biological role of ZNF32 and identify potential immunotherapy targets in cancer, we conducted an in-depth analysis of ZNF32. We comprehensively investigated the expression of ZNF32 across tumors using diverse databases, including TCGA, CCLE, TIMER2.
View Article and Find Full Text PDFAntioxid Redox Signal
January 2025
Department of Physiology, School of Basic Medical Sciences, Cheeloo College of Medicine, Shandong University, Jinan, People's Republic of China.
Hypoxia ischemia (HI) is a leading cause of cerebral palsy and long-term neurological sequelae in infants. Given that mitochondrial dysfunction in neurons contributes to HI brain damage, this study aimed to investigate the regulatory role of miR-9-5p in mitochondrial function following HI injury. Overexpression of miR-9-5p in HI mice or HO-exposed PC12 cells suppressed neuronal injury, associated with increased mitochondrial copy number, normalizing mitochondrial membrane potential, improved nuclear factor-erythroid factor 2-related factor 2 (Nrf2) activation, and downregulation of Keap1.
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