What We Talk About When We Talk About “Junk DNA”

Fagundes, Nelson J. R.; Bisso‐Machado, Rafael; Figueiredo, Pedro I. C. C.; Varal, Maikel; Zani, André

doi:10.1093/gbe/evac055

Cited by 16 publications

(9 citation statements)

References 41 publications

(65 reference statements)

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Almost 50% of the human genome is made up of repetitive DNA that does not encode proteins. 50 These DNA sequences are often considered to be "junk DNA" in the human genome. 50 Research has shown that one of the junk DNA sequences, VNTR2-1, actually functions to enhance telomerase gene activity and that the telomerase gene is more active in people with longer VNTR2-1 sequences.…”

Section: Genomic Instabilitymentioning

confidence: 99%

“…50 These DNA sequences are often considered to be "junk DNA" in the human genome. 50 Research has shown that one of the junk DNA sequences, VNTR2-1, actually functions to enhance telomerase gene activity and that the telomerase gene is more active in people with longer VNTR2-1 sequences. 51 Notably, however, a shorter sequence does not necessarily mean a shorter lifespan.…”

Section: Genomic Instabilitymentioning

confidence: 99%

See 1 more Smart Citation

Aging and aging-related diseases: from molecular mechanisms to interventions and treatments

Guo

Huang

Dou

et al. 2022

Sig Transduct Target Ther

480

160

View full text Add to dashboard Cite

Aging is a gradual and irreversible pathophysiological process. It presents with declines in tissue and cell functions and significant increases in the risks of various aging-related diseases, including neurodegenerative diseases, cardiovascular diseases, metabolic diseases, musculoskeletal diseases, and immune system diseases. Although the development of modern medicine has promoted human health and greatly extended life expectancy, with the aging of society, a variety of chronic diseases have gradually become the most important causes of disability and death in elderly individuals. Current research on aging focuses on elucidating how various endogenous and exogenous stresses (such as genomic instability, telomere dysfunction, epigenetic alterations, loss of proteostasis, compromise of autophagy, mitochondrial dysfunction, cellular senescence, stem cell exhaustion, altered intercellular communication, deregulated nutrient sensing) participate in the regulation of aging. Furthermore, thorough research on the pathogenesis of aging to identify interventions that promote health and longevity (such as caloric restriction, microbiota transplantation, and nutritional intervention) and clinical treatment methods for aging-related diseases (depletion of senescent cells, stem cell therapy, antioxidative and anti-inflammatory treatments, and hormone replacement therapy) could decrease the incidence and development of aging-related diseases and in turn promote healthy aging and longevity.

show abstract

Section: Genomic Instabilitymentioning

confidence: 99%

Section: Genomic Instabilitymentioning

confidence: 99%

Aging and aging-related diseases: from molecular mechanisms to interventions and treatments

Guo

Huang

Dou

et al. 2022

Sig Transduct Target Ther

480

160

View full text Add to dashboard Cite

show abstract

“…The complexity and adaptability of biological systems often find their roots in the ever-budding genetic landscape. Central to this is the emergence of de novo genes -- genes that arise from regions of DNA once categorized as ’junk’ and considered functionally insignificant (Fagundes, et al 2022; Ohno 1972). The birth of de novo genes was deemed impossible or functionally irrelevant (Jacob 1977; Mayr 1982).…”

Section: Introductionmentioning

confidence: 99%

One million years of solitude: the rapid evolution of de novo protein structure and complex

Chen,

Li,

Xia

et al. 2023

Preprint

View full text Add to dashboard Cite

Recent studies have established that de novo genes, evolving from non-coding sequences, enhance protein diversity through a stepwise process. However, the pattern and rate of their structural evolution over time remain unclear. Here, we addressed these issues within a short evolutionary timeframe (∼1 million years for 97% of rice de novo genes). We found that de novo genes evolve faster than gene duplicates in the intrinsic disordered regions (IDRs, such as random coils), secondary structural elements (such as α-helix and β-strand), hydrophobicity, and molecular recognition features (MoRFs). Specifically, we observed an 8-14% decay in random coils and IDR lengths per million years per protein, and a 2.3-6.5% increase in structured elements, hydrophobicity, and MoRFs. These patterns of structural evolution align with changes in amino acid composition over time. We also revealed significantly higher positive charges but smaller molecular weights for de novo proteins than duplicates. Tertiary structure predictions demonstrated that most de novo proteins, though not typically well-folded on their own, readily form low-energy and compact complexes with extensive residue contacts and conformational flexibility, suggesting “a faster-binding” scenario in de novo proteins to promote interaction. Our findings illuminate the rapid evolution of protein structure in the early life of de novo proteins in rice genome, originating from noncoding sequences, highlighting their quick transformation into active, complex-forming components within a remarkably short evolutionary timeframe.

show abstract

“…Another advantage is that each paralog encodes an N-terminal tail (NTT); so, the resulting NTTs have substantial differences in amino acid sequences [ 51 ], thus maintaining their stoichiometric relationship with partners in multicomponent interactions in changing external conditions [ 48 , 57 ]. As Fagundes et al opine, if a genetic element (the βCENH3 gene in our case) supports the organism’s adaptive level, it is qualified as functional and its “supporting function” is a proper biological function [ 58 ].…”

Section: Gene Duplicationsmentioning

confidence: 99%

Genetic Redundancy in Rye Shows in a Variety of Ways

Вершинин

Elisafenko

Евтушенко

2023

Plants

View full text Add to dashboard Cite

Fifty years ago Susumu Ohno formulated the famous C-value paradox, which states that there is no correlation between the physical sizes of the genome, i.e., the amount of DNA, and the complexity of the organism, and highlighted the problem of genome redundancy. DNA that does not have a positive effect on the fitness of organisms has been characterized as “junk or selfish DNA”. The controversial concept of junk DNA remains viable. Rye is a convenient subject for yet another test of the correctness and scientific significance of this concept. The genome of cultivated rye, Secale cereale L., is considered one of the largest among species of the tribe Triticeae and thus it tops the average angiosperm genome and the genomes of its closest evolutionary neighbors, such as species of barley, Hordeum (by approximately 30–35%), and diploid wheat species, Triticum (approximately 25%). The review provides an analysis of the structural organization of various regions of rye chromosomes with a description of the molecular mechanisms contributing to their size increase during evolution and the classes of DNA sequences involved in these processes. The history of the development of the concept of eukaryotic genome redundancy is traced and the current state of this problem is discussed.

show abstract

What We Talk About When We Talk About “Junk DNA”

Cited by 16 publications

References 41 publications

Aging and aging-related diseases: from molecular mechanisms to interventions and treatments

Aging and aging-related diseases: from molecular mechanisms to interventions and treatments

One million years of solitude: the rapid evolution of de novo protein structure and complex

Genetic Redundancy in Rye Shows in a Variety of Ways

Contact Info

Product

Resources

About