[metacognative]

Please give me a VERIFIABLE evolutionary fact.
Name one benefical mutation or evidence of a new species appearing in a hundred and fifty years of searching.
Note; DNA loss, as in bacterial immunity doesn't count nor do fruit flies with legs instead of antennae.

[Michael_Michaelangelo]

Please give me a VERIFIABLE evolutionary fact. Name one benefical mutation or evidence of a new species appearing in a hundred and fifty years of searching. Note; DNA loss, as in bacterial immunity doesn't count nor do fruit flies with legs instead of antennae.

You forgot primroses. :)

[stremba]

Of course those don't count. Show me evidence, but any evidence you have doesn't count.

[Modernman]

One beneficial mutation? Here you go:

http://www.cbc.ca/stories/2004/06/23/sci-tech/muscles040623

[NJ_gent]

Genetic mutations are an observable and verifiable fact. Genetic variation is an observable, verifiable fact. Natural selection is an observable, verifiable fact.

Evolution is the theory that describes what happens when they play together over a few million years under differing conditions. Your request to see masses of evidence from a 150-year time frame is ridiculous when the overall scope is in the millions of years for drastic evolutionary species divergence.

You did, however, ask for beneficial mutations. Here is a nice page laying out a bunch of beneficial mutations in just humans. If you look at the grand scale of all organisms, from bacteria to primates, you'll see a vast array of beneficial mutations that have been observed in the small time we've been looking. From that page, here are a couple:

"Lipoprotein lipase (LPL) is the rate-limiting enzyme in the lipolysis of triglyceride-rich lipoproteins, and the gene coding for LPL is therefore a candidate gene in atherogenesis. We previously demonstrated that two amino acid substitutions in LPL, the Asn291-Ser and the Asp9-Asn, are associated with elevated triglycerides and lower HDL cholesterol and are present with greater frequency in coronary artery disease (CAD) patients than in normolipidemic control subjects. Conversely, a third frequent mutation in this gene, the Ser447-Stop, is reported by some investigators to underlie higher HDL cholesterol levels and would represent a beneficial genetic variant in lipoprotein metabolism."

"These results demonstrate that a mutation in splice donor site of intron C can result in several variant mRNA transcripts and even permit partial correct splicing of FXIII mRNA. Further, even the minute amount of correctly processed mRNA is sufficient for producing protein capable of gamma-gamma dimerization of fibrin. This is a rare example of an inherited functional human disorder in which a mutation affecting splicing still permits some correct splicing to occur and this has a beneficial effect to the phenotype of the patients."

[NJ_gent]

I continue to look forward to your response.