India has long been an economic powerhouse, and today it's among the five fastest-growing economies. Several Make in India reforms led to this. The government's announcement of measures to boost the business environment in India has shifted the approach to governance. Make in India was introduced by Narendra Modi, India's prime minister, in 2014. The programme aims to increase India's manufacturing competitiveness and attract foreign investment. India's 100th rank shows that attempts to make it a manufacturing centre are paying off. India must overcome a few challenges to continue its winning streak. This article depicts and looks at the Make in India drive, which expects to change India into a monetary center point that draws in worldwide enterprises to contribute and create there. The examination uncovers its concerns, which upset its development. As a general rule, the review's discoveries support the production in India crusade, which means to make India a manufacturing hub. The data is assessed qualitatively utilizing the MAXQDA thematic software tool to arrive at on conclusion.
DNA hydroxymethylation (5hmC) is the most abundant oxidative derivative of DNA methylation (5mC) and is typically enriched at enhancers and gene bodies of transcriptionally active and tissue-specific genes. Although aberrant genomic 5hmC has been implicated in many age-related diseases, the functional role of the modification in aging remains largely unknown. Here, we report that 5hmC is stably enriched in multiple aged organs. Using the liver and cerebellum as model organs, we show that 5hmC accumulates in gene bodies associated with tissue-specific function and thereby restricts the magnitude of gene expression changes during aging. Mechanistically, we found that 5hmC decreases binding affinity of splicing factors compared to unmodified cytosine and 5mC, and is correlated with age-related alternative splicing events, suggesting RNA splicing as a potential mediator of the transcription restriction function of 5hmC. Furthermore, we show that various age-related contexts, such as prolonged quiescence and senescence, are partially responsible for driving the accumulation of 5hmC with age. We provide evidence that this age-related function is conserved in mouse and human tissues, and further show that the modification is altered by regimens known to modulate lifespan. Our findings reveal that 5hmC is a regulator of tissue-specific function and may play a role in regulating longevity.
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