Related Experiment Video
Updated: Jun 6, 2026
12:57
Investigating the Spreading and Toxicity of Prion-like Proteins Using the Metazoan Model Organism C. elegans
Published on: January 8, 2015
The prion hypothesis: from biological anomaly to basic regulatory mechanism
1Kent Fungal Group, School of Biosciences, University of Kent, Canterbury, Kent CT2 7NJ, UK. M.F.Tuite@kent.ac.uk
Nature Reviews. Molecular Cell Biology
|November 18, 2010
Summary
Fungal prions, unlike disease-causing mammalian prions, act as epigenetic factors influencing cellular functions. Their study reveals prions may be a widespread regulatory mechanism in biology.
Area of Science:
- Biochemistry
- Molecular Biology
- Genetics
Background:
- Prions are infectious proteins typically linked to fatal neurodegenerative diseases in mammals.
- The existence of fungal prions, which are non-pathogenic, challenges the traditional view of prions.
- This necessitates a re-evaluation of prions' role in cellular physiology.
Purpose of the Study:
- To explore the nature and function of fungal prions.
- To investigate the implications of fungal prions for understanding prion biology.
- To consider prions as a potential regulatory mechanism.
Main Methods:
- Comparative analysis of prion structures and propagation mechanisms in mammals and fungi.
- Investigation of cellular processes affected by fungal prions, such as metabolism and gene expression.
- Phenotypic analysis of cells harboring fungal prions.
Main Results:
- Fungal prions function as epigenetic determinants, altering cellular processes.
- These prions can modify metabolism and gene expression pathways.
- Prion-associated phenotypes were observed in fungal systems.
Conclusions:
- Fungal prions offer a new perspective on prion biology, distinct from disease association.
- Mechanistic similarities suggest prions could be a fundamental regulatory system.
- Prions may represent a newly appreciated, potentially ubiquitous, biological regulatory mechanism.
Related Concept Videos
03:03Amyloid Fibrils
Amyloid fibrils are aggregates of misfolded proteins. Under most circumstances, misfolded proteins are either refolded by chaperone proteins or degraded by the proteasome. However, in the case of a mutation or a disease, these proteins can accumulate to form large clusters and often further assemble to form elongated fibers, called fibrils.
Amyloid deposits were observed as early as 1639 in the liver and the spleen. In 1854, Rudolph Virchow performed iodine staining, normally used to...
Amyloid deposits were observed as early as 1639 in the liver and the spleen. In 1854, Rudolph Virchow performed iodine staining, normally used to...
03:03Amyloid Fibrils
Amyloid fibrils are aggregates of misfolded proteins. Under most circumstances, misfolded proteins are either refolded by chaperone proteins or degraded by the proteasome. However, in the case of a mutation or a disease, these proteins can accumulate to form large clusters and often further assemble to form elongated fibers, called fibrils.
Amyloid deposits were observed as early as 1639 in the liver and the spleen. In 1854, Rudolph Virchow performed iodine staining, normally used to...
Amyloid deposits were observed as early as 1639 in the liver and the spleen. In 1854, Rudolph Virchow performed iodine staining, normally used to...
01:37Neural Regulation
Digestion begins with a cephalic phase that prepares the digestive system to receive food. When our brain processes visual or olfactory information about food, it triggers impulses in the cranial nerves innervating the salivary glands and stomach to prepare for food.
01:29Biological Causes of Schizophrenia
Schizophrenia, a severe psychiatric disorder, arises from a complex interplay of biological factors, including genetic predisposition, structural brain abnormalities, neurotransmitter dysregulation, and developmental irregularities. These factors collectively contribute to the onset and progression of the disorder, which typically manifests in late adolescence or early adulthood.
Genetic Factors in Schizophrenia
The genetic basis of schizophrenia is strongly supported by family and twin studies.
Genetic Factors in Schizophrenia
The genetic basis of schizophrenia is strongly supported by family and twin studies.
01:24Parkinson Disease ll: Pathophysiology
Parkinson disease (PD) is a progressive neurodegenerative disorder primarily affecting movement, with additional non-motor features. Its pathophysiology involves complex interactions among genetic susceptibility, environmental exposures, and cellular dysfunction, including dopaminergic neuron loss, protein aggregation, and mitochondrial impairment.Selective NeurodegenerationA key feature is the degeneration of dopaminergic neurons in the substantia nigra pars compacta, leading to reduced...
01:27Psychosis: Pathophysiology of Schizophrenia and Other Psychotic Disorders
Schizophrenia is a neurodevelopmental disorder whose origins are rooted in complex genetic components. Despite our burgeoning understanding, the pathophysiology of this disorder remains incompletely deciphered.
Researchers have identified genetic factors that increase susceptibility to schizophrenia, underscoring the intricate interplay between genetics and environment in disease development. At the core of schizophrenia's pathophysiology is excessive dopaminergic neurotransmission within the...
Researchers have identified genetic factors that increase susceptibility to schizophrenia, underscoring the intricate interplay between genetics and environment in disease development. At the core of schizophrenia's pathophysiology is excessive dopaminergic neurotransmission within the...