[Since the conference room does not have WiFi, I'll have to just "pseudo-liveblog" this thing, and then post it when I get back to my room :) ]
[The first session I'm going to is Kevin Anderson's "A Creationist Perspective of Beneficial Mutations in Bacteria". All my own comments are in brackets]
Advantages of studying bacteria:
Significant features of bacterial genome:
Many of these features were thought to only exist in higher organisms, but have been found in at least E. Coli.
Mutations maintain diversity through mutation. Bacteria have ability to intentionally mutate their genome.
Mechanisms:
"Beneficial" Mutations
Wild Type + mutant => (a) more fit, (b) less fit, (c) neutral - can be any one of these
Study of E. Coli after 20,000 generations (Lenski)
Lenski 1999 - mutant stains possessed 50% greater "relative" fitness compared to parent (for the given environment).
Schneider et al 200 and Cooper et al 2001 - the beneficial mutants were the result of genetic disruptions (knockouts) - i.e. they were all degenerative
IS Element activates promoter to provide expression of a gene.
IS Element might also have an active repressor which disrupts it.
spoT mutants -> decreased ppGpp -> increased tRNA and rRNA -> increases protein synthesis - starts with a disruption or reduction of the cell's control mechanism
Mutants were less fit in other environments, such as different temperatures.
Conclusions of Lenski's long-term adaptation study:
Stress Survival
Increase temperature of E. Coli - get lots of mutants with gene duplications and deletions - genes involved in coping with higher temperature are the ones duplicated!
(Richle et al 2001, PNAS; Richle et al 2003 Physiol. Genom.; Richle et al 2005, Physiol. Biochem. Zool.)
Other studies show that when you return organism back to normal temperatures, duplications are removed [other studies not speicfied]
Antibiotic/antimicrobial resistance Mechanisms:
Common mechanisms
MarA/B System
MarR - represses promoter so that marA and marB are not expressed
Mutant to MarR is repressed, marA becomes a promoter for the promoter region, which increases the system, and forms both marA and marB, which then becomes marAB.
Metroindazole activation - [could not follow this one quickly]
Erythromycin resistance in e. coli - loss of 11 bp segment of 23S RNA
Kanamycin resistance in E. coli [slide up too short to complete]
Anderson 2005 CRSQ has a list of phenotype resistance and genotypes, and shows the degenerative nature of genotype systems.
Bacterial Response to Starvation
Glucose-limited adaptation - two mutant organisms that work together: [these are two different mutants in different cells I think]
Hypermutations - impaired repair mechanisms - increases chance of "beneficial" mutations under stress conditions.
[PROBLEM - keeps on banging the "beneficial but degenerative" drum]
Adaptive Mutation
Directed or random? - talked more by Georgia on Wednesday
Cultivation of Lac- in medium with lactose as sole catabolite. Frameshift reversal occurs at a much higher than random rate.
Possible mechanisms:
Nylon Degradation - Nylon-degrading bacteria identified in 1980s. Assumed as the evolution of a new metabolic pathway. Most-commonly studied - Anthrobacter sp. K172. Ei (NylA) EII (NylB) EIII (NylC) - on plasmid
Carboxyesterase - original version will not metabolize nylon. EII has an active site has broadened specificity to process Nylon. Broadening specificity of enzymes is a degenerative process. Prediction - EI and EIII will be found to be a degenerative (broadening specificity) mutation. Same prediction for opp protein in his next example for transport proteins.
Several mutations at once, but all degenerative.
Citrate evolution after 30,000 generations. E. Coli in aerobic conditions cannot process citrate. Lenski has found E. Coli that can process citrate. NOTE - genetics of this has not been studied - only phenotype.
Perhaps all Enterobacteria are all same created kind. [Interesting!]
citT (citrate transporter) is expressed anaerobically. If citT is cloned into a shuttle vector (Martinus et al. 1998 - J. Bacteriol), E. Coli can utilize citrate aerobically. The only thing that needs to be done is activating or derepressing the gene. The only mutation may be the loss of citT regulation! [Superinteresting!]
Antagonistic Pleiotropy - Analogy of "beneficial" mutations to constructing a house - removing non-supporting walls to create a larger dining room. Lose a room, but gain a function. Doesn't explain how the house is constructed.
Creation Model - Rigid Flexibility - flexibility that goes only so far.
Bacteria can often get back to wild type by recovering systems.
Q&A Time
Pennicilinase - only possible example of antibiotic resistance that has a chance of not being degenerative
Reversion - either genotypically - specific mutation reverts back, or phenotypically - a suppressor and then a repressor mutant.
Why is losing specificity a loss of ability, especially if V(max) of enzyme is not affected? Metabolism is managed by having very specific, narrow metabolic pathways, and showing a decrease in specificity will only cause long-term problems if compounded, because metabolics require tight specificity.
In debate, need to force evolution to show why the mechanisms they have examples for can contribute to large-scale evolution. If the mechanism is deregulation, then it can't be the source for novelty.
No current research on limits of baramins but there probably needs to be.
Why is it called "antagonistic pleiotropy" - seems to not be using "pleiotropy" in the strictest sense, but that's what the evolutionists have called it.
Isn't the reversion an increase in specificity? Couldn't other mutations increase specificity? There's no example of it occurring. [Isn't SMH in immunoglobulins an example of increasing specificity?]
[I think it was a good presentation, but I think he beat the degenerative drum WAY too much. My BSG presentation should indicate some ways in which organisms could theoretically produce increased specificity non-degeneratively (though there is always a tradeoff somewhere).]
[The second session I'm going to is Bob Hill's "The Tectonics of Venus and Creation"]
Venus as a prototype of Plate Tectonics - this is a review of secular literature in order to get it into the Creation literature. There are arguments for and against catastrophic plate tectonics in Venus. This is just the "pro" side in order to get the information into creationary literature.
Introduction
From radar, Venus looks a little like the earth, but drained of its oceans
Magellan - radar-mapped 98% of surface
Geologic Structures on Venus
Possible Implications
Venusian interior seems to have core, mantle, and crust.
Tectonic Model
Creationary Implications
Q&A
What are Corona? Not found elsewhere. Possible explanation (based only on photographs) Two layers of rock. magma is injected between the two layers, lifting one layer up. It later drains and drops back down, leaving circular faulting.
Are there any structures on venus which are analogous to terrestrial structures like subduction zones? A few proposed, all hotly debated. The ones found don't look that much like subduction zones. Need more space probes!
Why would Venus have lid tectonics and the earth plate tectonics? Really unknown.
Did Earth have impacts at the same time as Venus? Probably, but we have weather but Venus doesn't.
Is there evidence from a young-earth timescale of a resurfacing event? Not much except it matches Catastrophic Plate Tectonics.
Faulkner has suggested two cratering events suggested.
Surface temperature of venus is fairly uniform throughout. Atmosphere keeps it going.
Uniform randomness is unique to Venus. What about Mercury? Currently looks nonrandom, but not enough mapping done. If Mercury is nonrandom, it indicates that there may in fact have been a recent (during/post-flood) resurfacing event on Venus but not elsewhere. [Very interesting!]
[Very interesting stuff!!! Certainly at the beginning of understanding, but it looks promising]