Programmed cell death (PCD) is a genetically controlled pathway that plants can use to selectively eliminate redundant or damaged cells. In addition to its fundamental role in plant development, PCD can often be activated as an essential defense response when dealing with biotic and abiotic stresses. For example, localized, tightly controlled PCD can promote plant survival by restricting pathogen growth, driving the development of morphological traits for stress tolerance such as aerenchyma, or triggering systemic pro-survival responses. Relatively little is known about the molecular control of this essential process in plants, especially in comparison to well-described cell death models in animals. However, the networks orchestrating transcriptional regulation of plant PCD are emerging. Transcription factors (TFs) regulate the clusters of stimuli inducible genes and play a fundamental role in plant responses, such as PCD, to abiotic and biotic stresses. Here, we discuss the roles of different classes of transcription factors, including members of NAC, ERF and WRKY families, in cell fate regulation in response to environmental stresses. The role of TFs in stress-induced mitochondrial retrograde signaling is also reviewed in the context of life-and-death decisions of the plant cell and future research directions for further elucidation of TF-mediated control of stress-induced PCD events are proposed. An increased understanding of these complex signaling networks will inform and facilitate future breeding strategies to increase crop tolerance to disease and/or abiotic stresses.
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http://dx.doi.org/10.3389/fpls.2020.01235 | DOI Listing |
Mol Med
January 2025
Center for Autoimmune Musculoskeletal and Hematopoietic Diseases, Institute of Molecular Medicine, The Feinstein Institutes for Medical Research, Northwell Health, 350 Community Drive, Manhasset, New York, 11030, USA.
Background: The process of B cell activation and plasma cell (PC) formation involves morphological, transcriptional, and metabolic changes in the B cell. Blocking or reducing PC differentiation is one approach to treat autoimmune diseases that are characterized by the presence of pathogenic autoantibodies. Recent studies have suggested the potential of myricetin, a natural flavonoid with anti-inflammatory and antioxidant properties, to block or reduce PC differentiation.
View Article and Find Full Text PDFTrop Anim Health Prod
January 2025
Department of Biology, College of Science, Sultan Qaboos University, PC. 123, Muscat, Sultanate of Oman.
Bluetongue virus (BTV) has emerged as a significant concern in Oman, affecting various animal species, including camels. This cross-sectional study aimed to assess the seroprevalence of BTV in camels and explore the associated risk factors within the northern region of Oman. Between October 2016 and March 2017, 439 serum samples and 100 blood samples were collected from camels in five governorates.
View Article and Find Full Text PDFCell Mol Life Sci
January 2025
Department of Endocrinology, Central South University Third Xiangya Hospital, Changsha, China.
Pancreatic β-cell damage is a critical pathological mechanism in the progression of obese type 2 diabetes mellitus (T2DM). However, the exact underlying mechanism remains unclear. We established an obese T2DM mouse model via high-fat diet feeding.
View Article and Find Full Text PDFPlant Cell Rep
January 2025
Engineering Research Center of National Forestry and Grassland Administration for Rosa Roxburghii, Agricultural College, Guizhou University, Guiyang, 550025, People's Republic of China.
RrUNE12 binds to the RrGGP2 promoter to facilitate biosynthesis of AsA in Rosa roxburghii fruit. Furthermore, RrUNE12 upregulates antioxidant-related genes and maintains ROS homeostasis, thereby improving tolerance to salt stress. L-ascorbic acid (AsA) plays an essential role in stress defense as a major antioxidant in plant cells.
View Article and Find Full Text PDFCommun Biol
January 2025
Xianghu Laboratory, College of Life Sciences, Zhejiang University, Hangzhou, China.
Carbon catabolite repression (CCR) and de-repression (CCDR) are critical for fungal development and pathogenicity, yet the underlying regulatory mechanisms remain poorly understood in pathogenic fungi. Here, we identify a serine/threonine protein phosphatase catalytic subunit, Pp4c, as essential for growth, conidiation, virulence, and the utilization of carbohydrates and lipids in Magnaporthe oryzae. We demonstrate that the protein phosphatase 4 complex (Pp4c and Smek1 subunits), the AMP-activated protein kinase (AMPK) Snf1, and the transcriptional regulators CreA (repressor) and Crf1 (activator) collaboratively regulate the utilization of non-preferred carbon sources.
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