Presentation on theme: "Oct 15 3000-'13-3d. Exam and grades Why is percentile more useful than percentage? How to interpret your %ile: about 33-35 is the C/B line Depends in."— Presentation transcript:
Oct 15 3000-'13-3d
Exam and grades Why is percentile more useful than percentage? How to interpret your %ile: about 33-35 is the C/B line Depends in part on distribution, how wide variance
is the wiki helping you? has evolved into a resource for alternate explanations many interesting studies posted there, hasn’t quite taken on life of its own...
might i suggest... don’t be passive learners. alternate explanations good; explaining it to yourself and others is better. get into arguments! edit over each others stuff to make it better!
antibiotic resistance can it be reversed?
less than half the time when no antibiotic present, wild-type (sensitive) bacteria have higher fitness but still often lost to drift resistant bacteria have multiple “compensatory” pathways for minimizing fitness difference
w 11 =1, w 12 =0.95, w 22 =0.9 so the antibiotic resistant/susceptible work fits with what we have learned before about drift vs. selection, among other things!
where we are going we have today and 3 more lectures before exam 3 on 10/29 adaptation (chapter 10) and sex (chapter 11) are my goals read. do problems at end of chapter. come to class. go to discussion (remember this is 4 credit hours). contribute thoughtfully to wiki.
adaptation now we are talking about the evolution of complex traits - not just quantitative, but multi-factor, different parts working together (“complex adaptation”) sometimes new gene functions (following gene duplication, for example), sometimes co-opting existing functions interaction of multiple genes and gene regulatory networks
evolution in the lab Lenski experiment with multiple lines of E. coli growing in lab for 20 years
evolution in the lab Lenski experiment with multiple lines of E. coli growing in lab for 24 years that is 55000 generations! 2008: 31,000 generations in, one flask grew faster because it was using citrate for food *a defining feature of E. coli : they can’t eat citrate!
evolution in the lab actually E. coli can eat citrate, but only in O 2 -free environments: switches on citT gene, helps exchange one compound for citrate around generation 31,500 one bacterium accidentally duplicated citT, new copy near a switch that is “on” in presence of O 2 eventually duplication of THIS arrangement improved metabolic ability
evolution in the lab here’s the cool part: go back into the freezer prior to generation 31,500 bacterial stocks AFTER generation 20,000 restarted in long- term experiment; some of them evolved citrate metabolism prior to 20,000: nada if they supply post-20k stocks with a plasmid that carries citT+O2 switch, it can eat citrate. pre-20k stocks: nada another mutation was required that ALLOWED the second mutation to work!
“ It’s remarkable how this experiment contains many elements of evolution that scientists have noted in other species. It’s common for genes to get duplicated, and for the new copy to be rewired for a new job. Snake venom, to pick one example, also evolved when genes were accidentally copied and then rewired. A gene that originally produced a digestive enzyme in the pancreas, for instance, now started making that enzyme in a snake’s mouth. It turned out to be a crude but effective venom. Later mutations fine- tuned the new venom gene until it became wickedly good. The only important difference is that it took millions of years for snakes to evolve their arsenal of venoms, and scientists can only reconstruct their evolution by comparing living species. But in the case of E. coli, the transition unfolded fast enough for someone to track it from start to finish–and restart it when necessary. ” -Carl Zimmer (one of the text authors)
general case: gene duplication paralog: distinct gene regions of homologous origin in same genome
paralogy in snake venom
identifying gene duplication species A species B species C outgroup true phylogeny species A species B species C outgroup sequence genes species A species B species C outgroup duplication! species B species C
“pre-adaptations”: some changes seem small but needed for the “big” changes to happen many changes leading to evolution of venom
gene regulation duplication and mutation are one mechanism; changing how, when, where a gene turns on is probably more important language: cis is Latin for “same side of”; trans is Latin for “across from” cis-regulatory regions are stretches of DNA near to/attached to the gene in question; trans-regulation involves a product from elsewhere in genome
so is cis or trans affecting regulation of gene X? both. cis-regulatory regions are the portion of genome attached to a gene that INTERACT with environment (small scale!) to determine on/off status of gene the environment is defined by trans- regulatory elements: gradients of proteins and other products in tissue of organism
even-skipped gene segmentally-expressed genes important for modular development of many organisms
3 gains2 gains, 2+ losses1 gain, 3+ losses understanding phylogeny helps us understand our own development! 3 hypotheses for segmentation
Metazoans phylogeny work in progress MANY More genes
how it works: cis regions turn on given gradient in trans agents
patterning from external environment to embryo copies of gene and regulatory region in cells along axis of body diffusion gradient of trans-reg factor
evolution of development the role of regulatory elements in development of traits, body plans may be subtle: new metabolic pathways used may be profound: entirely distinct body plan “evo devo”