Alternative splicings (very technical)

From time to time I try to update my knowledge base on specific aspects included in my model. Here is the link to an open access article that may be of interest to others who want to learn more about biologically based cause and effect. This is not the type of information that you are likely to see in news reported by science journalists.

Intragenic DNA methylation modulates alternative splicing by recruiting MeCP2 to promote exon recognition

Excerpt 1) DNA methylation and MeCP2 binding are likely to influence pre-mRNA splicing patterns directly. In addition, nucleosome positioning has been suggested to play a role in pre-mRNA splicing31.

Excerpt 2) Mutations in the gene encoding MeCP2 primarily account for the debilitating neurodevelopmental disorder Rett syndrome (RTT), an autism spectrum disorder33,34. Mouse models of RTT exhibit RNA splicing defects22; however, whether these defects are relevant to human disease has yet to be investigated. Misregulation and sequence variants of MeCP2 are found in patients with autism spectrum disorders23,35 and the autoimmune disorder systemic lupus erythematosus36, respectively. Abnormal DNA methylation contributes to the etiology of these diseases37,38,39. Our study implicates the loss of function of DNA methylation and MeCP2 as a cause of altered pre-mRNA splicing, which could potentially contribute to disease development40, a possibility that warrants further investigation.

My comment: It will not get much clearer. Mutations cause disorders and diseases by altering pre-mRNA splicing.

Typically, alternative splicings are epigenetically controlled.

Control is good.

Mutations are bad.

Questions for theorists and philosophers.

1) What controls alternative splicings so that mutations do not perturb adaptations to the environment?

2) What made you think that mutations cause the adaptations?

In my model, adaptations are nutrient-dependent and pheromone-controlled. Experimental support for my model is overwhelming. Experimental support for mutation-driven evolution does not exist.

Author: James Kohl

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