It's from the Royal Ontario Museum in Toronto. Wikipedia on Crurotarsans (spelling?) says nothing of it.
Crocodilian relatives that walked upright?
I seriously have trouble believing this. Can anybody shed some light?
It's from the Royal Ontario Museum in Toronto. Wikipedia on Crurotarsans (spelling?) says nothing of it.
It's from the Royal Ontario Museum in Toronto. Wikipedia on Crurotarsans (spelling?) says nothing of it.
Pleiotropy saves the day for evolving new genes
What is the origin of new genes? In order to do new stuff, new genes are needed. Where do they come from, then?
Horizontal gene transfer (HGT) - direct transfer of a gene from one organism to another - is rampant within bacteria, so they may gain new function this way. However, that does not explain how the gene came to be in the first place.
Neofunctionalization: If the function is carried out by the original, the copy is free to evolve a new function by point mutations (etc.). However, such copies are much more likely to degrade by those mutations and lose the original function, thereby becoming a pseudogene.
Subfunctionalization: If the gene is pleiotropic, i.e. it has more than one function (expressed in more than one trait or cell-type or at different times), then the gene and its new copy can turn off gene expression differentially such that they share the set of functions. However this doesn't allow either much chance for evolving new function by mutation.
So what to do?
Näsvall et al. gave me this present for my 40th: Real-Time Evolution of New Genes by Innovation, Amplification, and Divergence.
They describe a new model/mechanism by which duplicated genes can retain the selection pressure to not succumb to deleterious mutations. They call it the innovation-amplification-divergene model (IAD).
IAD works like this: A gene initially has one function only (A). Then some genetic changes makes it also have a new function, b, which at first is not of too great importance. Then some environmental change favors the gene variants with the minor b-function (the innovation stage). This is then followed by duplication of the gene, such that there are now more than one copy that carries out A and b (the amplification stage). At this stage there is selection for more b, and at some point genetic changes in one of the copies results in a gene that is better at the new function, B. At this point, selection for the genes that do both A and b is relaxed, because the new gene (blue) carries out the new function. The original gene then loses the b function, and we are left with two distinct genes. Viola!
In other words, the green gene first becomes pleiotropic, is copied, followed by divergence, and then loss of pleiotropy. (How they could fail to mention pleiotropy in the article is beyond me.) The crucial feature is that at no point is the gene or any of the copes under no selection; there is always selection for them to be retained, so gene loss never occurs (pseudogenes are not created).
The researchers then look at a preexisting parental gene in Salmonella enterica that has low levels of two distinct activities that allows them to grow without the amino acids histidine and tryptophan, respectively.
Multiple evolutionary trajectories recovered through IAD. The x-axis indicates the HisA activity (assayed as growth rate in minimal glycerol medium with added tryptophan); the y axis indicates the TrpF activity (assayed as growth rate in minimal glycerol medium with added histidine). (A) Evolution of specialist enzymes (yellow) in which one activity is improved at the expense of the other. (B) Evolution of specialist enzymes (yellow) after initial evolution of a generalist enzyme (blue).
The figures here show how the generalist gene evolved to become specialists genes with increased function, doing better without both amino acids.
This is a model that explains how a gene with two functions can evolve to become two genes with distinct function under continued selection. It is this last part about selection that makes it novel, but it relies on the idea that the original gene had already evolved two distinct functions - that it was pleiotropic.
Näsvall J, Sun L, Roth JR, and Andersson DI (2012). Real-time evolution of new genes by innovation, amplification, and divergence. Science (New York, N.Y.), 338 (6105), 384-7 PMID: 23087246
Horizontal gene transfer (HGT) - direct transfer of a gene from one organism to another - is rampant within bacteria, so they may gain new function this way. However, that does not explain how the gene came to be in the first place.
Neofunctionalization: If the function is carried out by the original, the copy is free to evolve a new function by point mutations (etc.). However, such copies are much more likely to degrade by those mutations and lose the original function, thereby becoming a pseudogene.
Subfunctionalization: If the gene is pleiotropic, i.e. it has more than one function (expressed in more than one trait or cell-type or at different times), then the gene and its new copy can turn off gene expression differentially such that they share the set of functions. However this doesn't allow either much chance for evolving new function by mutation.
So what to do?
Näsvall et al. gave me this present for my 40th: Real-Time Evolution of New Genes by Innovation, Amplification, and Divergence.
They describe a new model/mechanism by which duplicated genes can retain the selection pressure to not succumb to deleterious mutations. They call it the innovation-amplification-divergene model (IAD).
IAD works like this: A gene initially has one function only (A). Then some genetic changes makes it also have a new function, b, which at first is not of too great importance. Then some environmental change favors the gene variants with the minor b-function (the innovation stage). This is then followed by duplication of the gene, such that there are now more than one copy that carries out A and b (the amplification stage). At this stage there is selection for more b, and at some point genetic changes in one of the copies results in a gene that is better at the new function, B. At this point, selection for the genes that do both A and b is relaxed, because the new gene (blue) carries out the new function. The original gene then loses the b function, and we are left with two distinct genes. Viola!
In other words, the green gene first becomes pleiotropic, is copied, followed by divergence, and then loss of pleiotropy. (How they could fail to mention pleiotropy in the article is beyond me.) The crucial feature is that at no point is the gene or any of the copes under no selection; there is always selection for them to be retained, so gene loss never occurs (pseudogenes are not created).
The researchers then look at a preexisting parental gene in Salmonella enterica that has low levels of two distinct activities that allows them to grow without the amino acids histidine and tryptophan, respectively.
Multiple evolutionary trajectories recovered through IAD. The x-axis indicates the HisA activity (assayed as growth rate in minimal glycerol medium with added tryptophan); the y axis indicates the TrpF activity (assayed as growth rate in minimal glycerol medium with added histidine). (A) Evolution of specialist enzymes (yellow) in which one activity is improved at the expense of the other. (B) Evolution of specialist enzymes (yellow) after initial evolution of a generalist enzyme (blue).
The figures here show how the generalist gene evolved to become specialists genes with increased function, doing better without both amino acids.
This is a model that explains how a gene with two functions can evolve to become two genes with distinct function under continued selection. It is this last part about selection that makes it novel, but it relies on the idea that the original gene had already evolved two distinct functions - that it was pleiotropic.
Pleiotropy comes from the Greek πλείων pleion, meaning "more", and τρέπειν trepein, meaning "to turn, to convert". It designates the occurrence of a single gene affecting multiple traits, and is a hugely important concept in evolutionary biology.Reference:
Näsvall J, Sun L, Roth JR, and Andersson DI (2012). Real-time evolution of new genes by innovation, amplification, and divergence. Science (New York, N.Y.), 338 (6105), 384-7 PMID: 23087246
Carnival of Evolution statistics
David Morrison just hosted Carnival f Evolution #52, and now he has written a post with lots of statistics of CoE: The network history of the Carnival of Evolution.
In short, we're doing quite well compared to many other carnivals who have gone extinct. This is especially true for science carnivals, of which CoE is the only active carnival listed on BlogCarnival.com.
The steady growth of CoE through time. "Fortunately, the number of posts has shown a steady upward curve, as indicated in the sixth graph, although not always at the one-blog-post-per-day rate set in the earliest days. However, over the past 20 Carnivals there has been an average of 1.06 blog posts cited per day of passing time, so we are certainly holding our own."
In short, we're doing quite well compared to many other carnivals who have gone extinct. This is especially true for science carnivals, of which CoE is the only active carnival listed on BlogCarnival.com.
The steady growth of CoE through time. "Fortunately, the number of posts has shown a steady upward curve, as indicated in the sixth graph, although not always at the one-blog-post-per-day rate set in the earliest days. However, over the past 20 Carnivals there has been an average of 1.06 blog posts cited per day of passing time, so we are certainly holding our own."
Titles in evolution - and in creation?
Here we go again with the new articles on evolution. This is just a very small sample that I chose out of interest from the last couple of weeks - and just from a few journals that I get eToCs sent from. In the meantime there has been nothing in Answers Research Journal, and I don't know where else to check. If you do, please let me know.
- Variation in personality and fitness in wild female baboons
- Biodiversity tracks temperature over time
- Epistasis as the primary factor in molecular evolution
- Aposematism and the Handicap Principle
- Turning Back the Clock: Slowing the Pace of Prehistory
- Physico-Genetic Determinants in the Evolution of Development
- The spatial architecture of protein function and adaptation
- Complex brain and optic lobes in an early Cambrian arthropod
- Crossing the threshold: gene flow, dominance and the critical level of standing genetic variation required for adaptation to novel environments
- Mutational meltdown in selfing Arabidopsis lyrata
- Aging: An Evolutionarily Derived Condition
- What could arsenic bacteria teach us about life?
- Genomic Variation in Natural Populations of Drosophila melanogaster
- Clonal Interference in the Evolution of Influenza
- Evolutionary Dynamics on Protein Bi-stability Landscapes can Potentially Resolve Adaptive Conflicts
- Criticality Is an Emergent Property of Genetic Networks that Exhibit Evolvability
Ochman on bacterial evolution
Yesterday I went to the annual Thomas S Whittam Memorial Lecture here at MSU. Howard Ochman talked about "Evolutionary Forces Affecting Bacterial Genomes", though he had changed the title to "Determinants of Genome Size and complexity.
Based on research in his lab had two conclusions about the evolution of bacterial genomes:
There are trends in the GC-content (amount of guanine and cytosize in the DNA) that differs among bacterial taxa. But closely related species have similar GC-content, and it turns out that genetic drift is not responsible for this, but that it is driven by selection. "Escherichia coli strains harboring G+C-rich versions of genes display higher growth rates" (Raghavan, 2012).
Genome size and abundance of pseudogenes correlates with the size of the effective population size: a larger Ne gives larger genomes, while smaller Ne results in smaller genomes. Pseudogene abundance is less straightforward, with the largest and smallest genomes and Ne both having few pseudogenes, but those intermediate in size having many.
References
Kuo CH, & Ochman H (2010). The extinction dynamics of bacterial pseudogenes. PLoS genetics, 6 (8) PMID: 20700439
Kuo CH, Moran NA, & Ochman H (2009). The consequences of genetic drift for bacterial genome complexity. Genome research, 19 (8), 1450-4 PMID: 19502381
Raghavan R, Kelkar YD, & Ochman H (2012). A selective force favoring increased G+C content in bacterial genes. Proceedings of the National Academy of Sciences of the United States of America, 109 (36), 14504-7 PMID: 22908296
Based on research in his lab had two conclusions about the evolution of bacterial genomes:
- Genome size is drifting
- GC-content is under selection
There are trends in the GC-content (amount of guanine and cytosize in the DNA) that differs among bacterial taxa. But closely related species have similar GC-content, and it turns out that genetic drift is not responsible for this, but that it is driven by selection. "Escherichia coli strains harboring G+C-rich versions of genes display higher growth rates" (Raghavan, 2012).
Genome size and abundance of pseudogenes correlates with the size of the effective population size: a larger Ne gives larger genomes, while smaller Ne results in smaller genomes. Pseudogene abundance is less straightforward, with the largest and smallest genomes and Ne both having few pseudogenes, but those intermediate in size having many.
References
Kuo CH, & Ochman H (2010). The extinction dynamics of bacterial pseudogenes. PLoS genetics, 6 (8) PMID: 20700439
Kuo CH, Moran NA, & Ochman H (2009). The consequences of genetic drift for bacterial genome complexity. Genome research, 19 (8), 1450-4 PMID: 19502381
Raghavan R, Kelkar YD, & Ochman H (2012). A selective force favoring increased G+C content in bacterial genes. Proceedings of the National Academy of Sciences of the United States of America, 109 (36), 14504-7 PMID: 22908296