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Apparently you were not in a course which dealt with the nitty-gritty of genetics. You were in a class that studied evolution and stated theories that have nothing to do with genetics. What you were told were lies.ScienceChic wrote: That's hilarious, considering that I trained as a geneticist.
It was one of the first disciplines to prove how changes could occur over time through mutation, genetic drift, punctuated equilibrium, and speciation. I highly recommend reading The Selfish Gene and The Extended Phenotype by Dawkins.
How are big picture pondering divorced from facts?
Renegade, my apologies for not getting back to you earlier. I do not think he intended the title as an insult at all, nor do I think he's trying to say that evolution occurred from nothing. Indeed, at the end of his writing, he said "But there's no reason for people of faith to reject the mountains of data and the evidence of their own senses. Reconciling is easy: Believe, if you want to, that God set up the rules of evolution among His wonders, along with the laws of physics, and probability, and everything else we can see and measure for ourselves."
Evolution does not attempt to answer the question of where/how everything began, it deals only with the process of how things have changed since then. There's not reason that a deity couldn't have created it as a system, and there's no reason that it couldn't just have occurred by following the laws of physics.
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Mutations in the Cu/Zn superoxide dismutase (SOD1) gene are responsible for 15-20% of familial amyotrophic lateral sclerosis (FALS) cases. Severity of the ALS phenotype is dependent on genetic background for mice carrying the mG86R SOD1 transgene. A BAC (149m19) containing several candidate genes (Serf, Smn, Naip2 and Naip5) and derived from 129Sv genomic DNA was used to investigate whether these genes partially rescue the mG86R SOD1 (FVB/NJ) ALS phenotype by delaying ALS onset. Two single-insertion BAC lines were produced and both mRNA and protein for BAC genes were shown to be elevated. Mice heterozygous for mG86R SOD1 and BAC149m19 in the FVB/NJ background were shown to have significantly delayed ALS onset compared to mG86R SOD1 controls. BAC 149m19 did not significantly delay ALS onset for mice carrying the human G93A SOD1 mutation in the FVB/NJ background. Delayed ALS onset for BAC/mG86R mice was not due to reduced SOD1 expression. Overexpression of one or more of the BAC genes appears to be linked to the severity of ALS phenotype in mice, but in a mutation specific manner.
Characterization of the genomic structure encoding the 5′ portion of rat Vr1 confirmed that VR.5′sv is derived from the VR gene; however, SIC seemed to be derived from two related but independent genes. We also deduced the genomic organization of the human gene VR1. Comparative studies of rat and human VR genes showed substantial conservation in genomic organization. The splice site flanking exon–intron 7 in rat and human VR1 diverged from the expected consensus sequence; this may help to explain the skipping of exon 7 within VR.5′sv and other VR splice variants.
Definition: Any alteration in a gene from its natural state; may be disease causing or a benign, normal variant.
A mutation is a change in a DNA sequence. Mutations can result from DNA copying mistakes made during cell division, exposure to ionizing radiation, exposure to chemicals called mutagens, or infection by viruses. Germ line mutations occur in the eggs and sperm and can be passed on to offspring, while somatic mutations occur in body cells and are not passed on.
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