Polyploidy as a Fundamental Phenomenon in Evolution, Development, Adaptation and Diseases
Abstract
:1. Introduction
2. Evolution
2.1. General Picture
2.2. Cellular and Molecular Aspects
2.3. Polyploidy in Agriculture and Aquaculture Biotechnology
3. Evolutionary Medicine
3.1. Ohnologs and Diseases
3.2. Polyploidy in Cancer
4. Somatic Polyploidy
4.1. Somatic Polyploidy Is a Way of Adaptation to Stress
4.2. Polyploid Cells Reduce the Functional Capacity of the Organ
4.3. Functional Load Can Control Polyploidization during Postnatal Organogenesis of Heart and Liver
5. Ploidy-Associated Transcriptome Features Are Related to Stress Response, Metabolism, Morphogenesis, and Longevity
5.1. Ploidy-Associated Transcriptomic Features Are Evolutionary Conserved
5.2. The Epigenetics of Ploidy-Associated Transcriptomic Features
6. Polyploidy Meets the Hallmarks of Developmental Programming of Adult Diseases in Slowly Renewing or Terminally Differentiated Organs
- Polyploidy helps to cope with the adverse environments via the augmentation of stress resistance and adaptation through epigenetic mechanisms [3,78,112]. Furthermore, it is one of the most variable characteristics of somatic cells. The degree of polyploidization in homologous organs shows large across-species diversity. The percentage of cardiomyocytes with polyploid nuclei varies several folds in mammals of similar weight. For example, about 50% of human cardiomyocytes contain nuclei with 4, 8, 16, or even 32 genomes, whereas cardiomyocytes of the grey wolf or reindeer show only about 1% of cells with polyploid nuclei [71,82]. Accordingly, cardiomyocyte ploidy also varies between individuals of the same species. The mean ploidy in the normal human heart varies from about 4× to 10× [77,100,108]. Thus, polyploidy is characterized by the degree of biologic plasticity similar to the renowned factors of ontogenetic programming.
- Polyploid cells (e.g., cardiomyocytes, megakaryocytes, hepatocytes, pancreacytes, vascular epithelial cells, retina epithelium) appeared in the perinatal and early postnatal ontogenesis [9]. These periods are characterized by high biological plasticity and coincide in time with the critical periods of development [131,132].
- Cells of slowly renewing organs, including neurons of neocortex and cerebellum, cardiomyocytes, and hepatocytes, which accumulate additional genomes in infancy, childhood, and pre-pubertant period, retain the increased genome amount throughout their lives, regardless of environmental conditions [9,72,77,100,145].
- Polyploidization is associated with a decrease in organ functional potential [71,82,104,109]. This decrease probably originates from the involvement of polyploidy in the trade-off between proliferation and function that is also a sign of the developmental programming of adult diseases factor [71,107,131].
- The level of ploidy, particularly in cardiomyocytes, responds to the well-established stimuli of developmental programming (including adverse growth conditions, increased functional load, inflammation, and malnutrition) similarly in the various species and various cells [9,71,132,141]. For example, in mammal hepatocytes, cardiomyocytes, retinocytes, and drosophila somatic cells, polyploidy is associated with the increased response to stress, activated pathways of morphogenesis and glycolytic metabolism, and the weakened aerobic metabolism and apoptosis [3,11,112,146].
- Polyploidy is associated with epigenetic changes at various levels of genome organization leading to chromatin remodeling and genome instability [95,123,124]. The association between polyploidy and chromatin decompactization under stress was well documented for cardiomyocytes and hepatocytes [76,128]. Polyploidy can alter global patterns of DNA methylation, microRNA expression, and histone modification in mammalian, insect, and plant cells [1,2,78,95,112,127,129]. Polyploid cells show higher expression of bivalent genes, which harbor both activating (H3K4me3) and repressive (H3K27me3) chromatin domains, allowing rapid switching between cellular programs [112]. Overall, ploidy-associated transcriptomic changes occur through the same epigenetic mechanisms as in the developmental programming of health and disease, including chromatin remodeling, DNA methylation, histone modification, and others.
Experimental Studies Confirm the Role of Polyploidy in the Developmental Programming of Health and Disease
7. Genome Duplication in Regeneration and Aging
8. Conclusions
Author Contributions
Funding
Informed Consent Statement
Data Availability Statement
Acknowledgments
Conflicts of Interest
References
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Anatskaya, O.V.; Vinogradov, A.E. Polyploidy as a Fundamental Phenomenon in Evolution, Development, Adaptation and Diseases. Int. J. Mol. Sci. 2022, 23, 3542. https://doi.org/10.3390/ijms23073542
Anatskaya OV, Vinogradov AE. Polyploidy as a Fundamental Phenomenon in Evolution, Development, Adaptation and Diseases. International Journal of Molecular Sciences. 2022; 23(7):3542. https://doi.org/10.3390/ijms23073542
Chicago/Turabian StyleAnatskaya, Olga V., and Alexander E. Vinogradov. 2022. "Polyploidy as a Fundamental Phenomenon in Evolution, Development, Adaptation and Diseases" International Journal of Molecular Sciences 23, no. 7: 3542. https://doi.org/10.3390/ijms23073542