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what are the most important genes in epitranscriptome regulation (yogesh saletore)
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what is the most control-sequence like of it
Among the hnRNP family, hnRNP A1 is the most closely associated with control-sequence-like regulatory activity in splicing. hnRNP A1 binds to exonic or intronic splicing silencers (ESS/ISS) and can directly inhibit the use of particular splice sites during regulated splicing events. This protein recognizes high-affinity RNA sequences such as UAGGGU (its consensus binding motif) and, through cooperative binding, can spread along RNA to cover control elements, efficiently repressing splice site selection.
Other hnRNPs with strong control-sequence activity include:
- hnRNP I (also known as PTBP1), which binds polypyrimidine tracts at intron branch points and represses or regulates alternate splice site usage.
- hnRNP H/F, which are crucial for splicing enhancer and silencer complex formation at specific exons, such as the c-src N1 exon, acting as master regulators of inclusion or exclusion.
However, hnRNP A1 stands out for its canonical binding to splicing silencer elements and its direct role in modulating exon inclusion or skipping through interaction with control sequences.
what are the most important genes in epitranscriptome regulation (yogesh saletore)
The most important genes in epitranscriptome regulation, as highlighted in work by Yogesh Saletore and others, are those involved in adding, reading, and removing RNA modifications—especially N6-methyladenosine (m^6A), the most abundant and well-studied epitranscriptomic mark in mammals. These genes fall into three key categories: writers, erasers, and readers.
Key Categories and Genes
Writers (Methyltransferases)
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METTL3: The central m^6A methyltransferase that catalyzes methylation, often with METTL14 as a heterodimer partner.
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METTL14: Works with METTL3 to “write” m^6A marks on mRNA.
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WTAP: A regulatory protein that guides METTL3/METTL14 complex to its RNA targets.
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Other writer genes: METTL16, responsible for m^6A in U6 snRNA and certain mRNAs.
Erasers (Demethylases)
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FTO: An m^6A demethylase that can “erase” epitranscriptomic marks and is implicated in metabolic regulation.
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ALKBH5: Removes m^6A, modulating RNA stability and splicing.
Readers (Binding Proteins)
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YTHDF1, YTHDF2, YTHDF3, YTHDC1, YTHDC2: These proteins recognize m^6A and mediate downstream regulatory effects, controlling RNA stability, translation, and nuclear export.
Other Major Modifications and Genes
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m^1A (N1-methyladenosine): Associated genes include TRMT61A and TRMT6, which catalyze this modification.
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m^5C (5-methylcytosine): NSUN2 and TRDMT1 enzymes are responsible for adding this modification.
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hm^5C (5-hydroxymethylcytosine): TET family proteins are linked to this mark.
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m^7G (7-methylguanosine) cap: RNMT and other cap methyltransferases mediate this modification.
Functional Impact
These genes and their products work in concert to dynamically regulate RNA metabolism, splicing, degradation, localization, and translation, making them critical for development and disease. Saletore and colleagues’ reviews emphasize the complexity and pervasiveness of these modifications across thousands of genes in mammalian cells.
In summary, top genes for epitranscriptome regulation are those encoding the m^6A writers (METTL3, METTL14, WTAP), m^6A erasers (FTO, ALKBH5), and m^6A readers (YTHDF/YTHDC family), along with enzymes for other major RNA modifications (NSUN2, TRDMT1, TRMT61A, TET).
is FTO obesity related?
Yes, the FTO gene is strongly associated with obesity risk. Genetic variants within the FTO gene, especially single-nucleotide polymorphisms (SNPs) like rs9939609, are consistently linked to higher body mass index (BMI) and increased likelihood of obesity in global populations, including both Western and Asian groups. Individuals with risk alleles in FTO tend to weigh more and are at a higher risk for developing obesity; for instance, carriers of two copies of the risk allele often weigh up to 3 kilograms (6.6 lbs) more with a 1.67-fold higher rate of obesity compared to individuals without the risk allele.
The biological mechanism involves FTO’s role as an m^6A RNA demethylase, which influences gene expression related to energy balance, appetite, and fat metabolism. FTO is highly expressed in areas of the brain like the hypothalamus, regulating appetite, satiety, and preferences for calorie-dense foods. Variants in this gene can alter dietary behaviors, leading to increased fat and carbohydrate intake, further raising the risk of obesity.
In summary, FTO is a critical epitranscriptomic regulator gene directly linked to human obesity risk through its effects on diet, energy regulation, and fat homeostasis.
what DNA repair genes are most associated with naked mole rats
The DNA repair gene most strongly associated with naked mole rats is cGAS (cyclic GMP-AMP synthase). Recent studies have revealed that a unique form of cGAS in naked mole rats, altered by only four specific amino acid substitutions, fundamentally changes its activity compared to that in other mammals. In humans and mice, cGAS typically suppresses the homologous recombination (HR) DNA repair pathway, which can lead to genomic instability and reduced repair efficiency. However, the naked mole rat version of cGAS enhances the HR pathway’s repair efficiency and helps maintain genome stability—likely contributing to their exceptional longevity and resistance to age-related diseases.
Additionally, naked mole rat cGAS enables a prolonged presence on chromatin after DNA damage. This facilitates the recruitment of key repair factors, notably RAD50 (an HR protein) and FANCI (from the Fanconi anemia pathway), further boosting double-strand break repair. The synergy between these proteins and the unique cGAS variant underlies the naked mole rat’s superior ability to repair DNA compared to other rodents.
In summary, naked mole rats’ exceptional DNA repair—and thus their longevity—is especially linked to:
- Modified cGAS (cyclic GMP-AMP synthase)
- Enhanced recruitment/activity of RAD50 (HR factor) and FANCI (Fanconi pathway factor).
These findings are considered major advances in understanding how DNA repair genes shape the naked mole rat’s unique biology and long life.
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