Alternative splicing of pre-mRNA

From Precis to Proof in 6000 years (3)

See first: Coulombic interactions facilitate polycombic adaptation
See also: From Precis to Proof in 6000 years (2)
See also: RNA catalyses nuclear pre-mRNA splicing 06 November 2013

…our data indicate that the spliceosome, like the ribosome44,45, uses RNA to effect catalysis in the context of a complex ribonucleoprotein assembly. Moreover, the common catalytic mechanism used by the spliceosome and group II introns is consistent with a common evolutionary origin between the spliceosome and these ancient RNA retroelements46,47. Our findings thus support the idea that modern ribonucleoprotein enzymes evolved from a primordial ‘RNA world’ (ref. 48), in which catalysis was performed exclusively by RNA.

My comment: Claims that everything “evolved” are rarely seen in the context of data that links RNA-mediated physics, chemistry, and molecular epigenetics from the spliceosome and ribosome to catalysis and the complexity ribonucleoprotein assembly.  But here, they claimed: “Our findings thus support the idea that modern ribonucleoprotein enzymes evolved…”
See for comparison: Substantial contribution of extrinsic risk factors to cancer development 16 December 2015
Abstract conclusion

…rates of endogenous mutation accumulation by intrinsic processes are not sufficient to account for the observed cancer risks. Collectively, we conclude that cancer risk is heavily influenced by extrinsic factors. These results are important for strategizing cancer prevention, research and public health.

See for comparison: Cancer studies clash over mechanisms of malignancy 16 December 2015


The authors also examined patterns in the mutations associated with certain cancers; ultraviolet light, for example, tends to create a tell-tale signature of mutations in DNA. And they used other mathematical models, expanding the data set used in the earlier work to include prostate and breast cancer — two of the most common cancers.

“There’s no question what’s at stake. This informs whether or not we expend energy on prevention.”

The models suggested that mutations during cell division rarely build up to the point of producing cancer, even in tissues with relatively high rates of cell division. In almost all cases, the team found that some exposure to carcinogens or other environmental factors would be needed to trigger disease.

My comment: Theories about mutation-driven evolution should have promptly been abandoned. Instead, this conference started on November 7, 2016: New trends in evolutionary biology: biological, philosophical and social science perspectives