Abstract
Methylation of adenosines at N6 position (m6A) is the most frequent internal modification in mRNAs of the human genome and attributable to diverse roles in physiological development, and pathophysiological processes. However, studies on the role of m6A in neuronal development are sparse and not well-documented. The m6A detection remains challenging due to its inconsistent pattern and less sensitivity by the current detection techniques. Therefore, we applied a sliding window technique to identify the consensus site (5′-GGACT-3′) n ≥ 2 and annotated all m6A hotspots in the human genome. Over 6.78 × 107 hotspots were identified and 96.4% were found to be located in the non-coding regions, suggesting that methylation occurs before splicing. Several genes, RPS6K, NRP1, NRXN, EGFR, YTHDF2, have been involved in various stages of neuron development and their functioning. However, the contribution of m6A in these genes needs further validation in the experimental model. Thus, the present study elaborates the location of m6A in the human genome and its function in neuron physiology.
Highlights
Introduction published maps and institutional affilAmong the 150 reported RNA modifications to date, methylation at N6 position of adenosine (m6A) is the post-transcriptional RNA modification with a high physiological relevance [1]
Chromosome 2, having 242 million base pairs (Mbps) nucleotides were found to carry the highest number of target sequences in total (n = 1014.79 × 104 )
The target sequences of 31.76 × 104, 541.56 × 104, 1.45 × 104, 433.77 × 104,and 6.23 × 104 Mbps were found in exonic, intronic, promoter, genomic, and downstream regulatory regions (DRR), respectively (Table 1, Figure 2a)
Summary
Among the 150 reported RNA modifications to date, methylation at N6 position of adenosine (m6A) is the post-transcriptional RNA modification with a high physiological relevance [1]. This reversible modification of RNA regulates the expression of several genes and affects human physiology [2]. Over 7000 genes have been reported to carry this modification in humans, and aberrant RNA modification contributes to the pathogenesis of various human diseases. The abnormal modification of human tRNA may lead to mental retardation and intellectual disability [3]. Altered m6A modifications have been linked with several diseases, such as obesity, cancer, diabetes mellitus, stress-related psychiatric disorders, neuronal development, and functions [4,5]. Several analytical tools have revealed that 50 -GGACU-30 is the most common structural signature for m6A modification [6,7]
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