1. Table 8.3 & Alberts Fig.1.38 EVOLUTION OF GENOMES C-value paradox: - in certain cases, lack of correlation between morphological complexity and genome size “[For] some commonly cited extreme values for amoebae... considerable uncertainty about the accuracy of these measurements and the ploidy level of the species...” Gregory Nature Rev. Genet. 6:699, 2005

2. Fig. 8.15 Genic fraction vs. genome size Function of non-genic DNA in eukaryotes? Gregory Nature Rev. Genet. 6:699, 2005 Composition of human genome

3. Hartwell Fig. 21.11 Genic contribution to expansion in genome size

4. Figure 8.7 Scenario showing possible events following whole genome duplication 26 genes on 2 chromosomes 36 genes on 4 chromosomes

5. Kellis Nature 428:617, 2004 Evidence for whole genome duplication in ancestor of yeast see also Fig.8.7 ~ 100 million years ago?

6. Frequency distribution of haploid chromosome numbers in dicot plants For chromosome number >12, even numbers much more common than odd numbers Griffiths 7 th ed, Fig. 26-12 Duplication of entire genome much more common in plant evolution than in animal evolutionary history

7. Fig. 6.25 Over evolutionary time expect independent mutations to accumulate Evolution of tandem arrays of eukaryotic genes … but often observe all copies identical (or nearly so) - evolve “in concert”

8. Concerted evolution - maintenance of homogeneous nt sequences among multi-gene family members (especially when in tandem arrays) - eg. eukaryotic ribosomal RNA gene copies - exchange of sequence info so members kept very similar Fig. 6.26

9. Fig. 6.27 Possible evolutionary scenarios resulting in “homogenized” tandem array 1. Beneficial mutations fixed by positive selection -but spacers with no known function show concerted evolution 2. Recent amplification 3. Mutation in one repeat “spreads” to others

10. Fig. 6.31 Unequal crossing over - homologous recombination between misaligned arrays - change in number of repeats

11. Example of unequal crossing over in human  globin array misalignment (of sister chromatids during mitosis in germ cell or homologous chromosomes during meiosis…) Page & Holmes Fig. 3.15 “Lepore”  thalassemia

12. Gene conversion - non-reciprocal recombination - no change in gene copy number - can occur in dispersed as well as tandem repeats Fig. 6.29 Watson Fig. 10-21 - example of yeast mating-type switching

13. Fig. 6.33 Exon 3 Exons 1 & 2 How do you interpret these data? Example of concerted evolution in primate  globin gene cluster... and panel 3 of Fig.6.33 ?

14. Fig. 6.33 PR pancreative ribonuclease SR seminal ribonuclease Resurrection of ribonuclease pseudogene by gene conversion What is predicted status of SR gene in giraffe? or sheep? … in some bovine species, gene conversion of  SR with PR gene, so functional again

15. Factors affecting rate of concerted evolution (p. 317-320) 1. Number, arrangement, structure of repeats 2. Functional requirement - selective advantage of high amount of same gene product vs. diversity 3. Population size - non-coding regions evolve more rapidly, and if divergent enough may “escape” homogenization - time for variant to be fixed or eliminated

16. Evolutionary implications of concerted evolution (p.320-322) 1. Spread of advantageous mutations (or removal of deleterious ones) 2. Retards paralogous gene divergence (preventing redundant copy from becoming non-functional) 3. Generates increased genetic variation at a particular locus within a population “molecular drive” Methodological implications - degree of sequence divergence of paralogous genes undergoing concerted evolution is not correlated with evolutionary time so gene duplications can appear younger than they really are…