Evolution (specifically, Intelligent Evolution)

Started by Deb, July 20, 2015, 10:48:02 PM

Previous topic - Next topic

Deb

Spoiler: Take-away from these experiments:

Evolution is a conscious choice and not a random effect.
Evolution (life-sustaining mutations) derives as a direct response to a traumatic environmental crisis.


From Bruce Lipton's Spontaneous Evolution, pages 241-244

Because evolution appeared to be driven solely by mutations, science concluded that randomly driven evolution has no purpose. The idea fit well with scientific materialism's belief in a purely materialistic Universe and helped shift the focus from intentional creation to merely a "throw of genetic dice." A human being is just another [of] the "accidental tourists" who materialized in the biosphere through random acts of heredity.

However, in 1988, internationally prominent geneticist John Cairns challenged science's established belief in random evolution. Cairns' novel research on bacteria, facetiously titled, "The origin of mutants," was published in the prestigious British Journal of Nature.

He chose bacteria with a crippled gene that made a defective version of the enzyme lactase needed to digest lactose, a sugar present in milk. He then inoculated these lactase-deficient bacteria into cultures in which the only nutrient was lactose. Unable to metabolize this nutrient, the bacteria could neither grow nor reproduce, so no colonies were expected to appear in any of the experiments. Yet, surprisingly, a large number of cultures expressed growth of bacterial colonies.

Sampling the bacteria he started with Cairns found that mutated forms did not exist in the original inoculum. Consequently, he concluded that lactase gene mutations followed, not preceded, their exposure to the new environment. Unlike the experiments of Luria and Delbruck, which relied on viruses killing the bacteria almost instantly, Cairns's experiment starved bacteria slowly. In other words, Cairns gave the stressed bacteria sufficient time to engage and activate innate mutation-producing mechanisms in order to survive.

In Carns's study, life-sustaining mutations appeared to derive as a direct response to a traumatic environmental crisis. Interestingly, further assays revealed that only the genes associated with lactose metabolism were affected. In addition, out of the five possible different mutation mechanisms, all of the surviving bacteria expressed the exact same type of mutation. Clearly, the results do not support the assumption of totally random mutations and purposeless evolution!

Cairns referred to this newly discovered mechanism as directed mutation. But the very idea that environmental stimuli could feed back into an organism and direct a rewriting of genetic information was an abomination to the central dogma, and the response from conventional science was swift and hostile....

Other the next decade, other researchers replicated Carns's results, which should have increased the credibility of his work. However, the scientific community still considered his notion to be shocking and unacceptable.

- - - - -
Report:
Genetic analysis of spontaneous lactose-utilizing mutants from vibrio vulnificus.
Baek CH1, Lee KE, Park DK, Choi SH, Kim KS.
http://www.ncbi.nlm.nih.gov/pubmed/18167454

Abstract
Wild-type V. vulnificus cannot grow using lactose as the sole carbon source or take up the sugar. However, prolonged culture of this species in media containing lactose as the sole carbon source leads to the generation of a spontaneous lactose-utilizing (LU) mutant. This mutant showed strong beta- galactosidase activity, whereas the wild-type strain showed a barely detectable level of the activity. A mutant with a lesion in a gene homologous to the lacZ of E. coli in the bacterium no longer showed beta-galactosidase activity or generated spontaneous LU mutants, suggesting that the lacZ homolog is responsible for the catabolism of lactose, but the expression of the gene and genes for transport of lactose is tightly regulated. Genetic analysis of spontaneous LU mutants showed that all the mutations occur in a lacI homolog, which is located downstream to the lacZ and putative ABC-type lac permease genes. Consistent with this, a genomic library clone containing the lacI gene, when present in trans, made the spontaneous LU mutants no longer able to utilize lactose as the sole carbon source. Taken together with the observation that excessive amounts of exogenously supplemented possible catabolic products of lactose have negative effects on the growth and survivability of V. vulnificus, we suggest that V. vulnificus has evolved to carry a repressor that tightly regulates the expression of lacZ to keep the intracellular toxic catabolic intermediates at a sublethal level.