Paul Draper is a philosopher at Purdue University (West Lafayette, Indiana, USA). He has just (Aug. 2, 2017) posted an article on Atheism and Agnosticism on the Stanford Encyclopedia of Philosophy website.
Many philosphers use a different definition of atheism than many atheists. Philosophers tend to define atheism as the proposition that god(s) do not exist. Many atheists (I am one) define atheism as the lack of belief in god(s). The distinction is important but for now I want to discuss Draper's defense of agnosticism.
Today is the Fête Nationale in France known also as "le quatorze juillet" or Bastille Day.This is the day in 1789 when French citizens stormed and captured the Bastille—a Royalist fortress in Paris. It marks the symbolic beginning of the French revolution although the real beginning is when the Third Estate transformed itself into the National Assembly on June 17, 1789 [Tennis Court Oath]. 1. I wonder if President Trump sang La Marseillaise while he was at the ceremonies today?
Check out Uncertain Principles for another version of La Marseillaise—this is the famous scene in Casablanca.
Reposted and modified from 2016.
The genetic load argument is one of the oldest arguments for junk DNA and it's one of the most powerful arguments that most of our genome must be junk. The concept dates back to J.B.S. Haldane in the late 1930s but the modern argument traditionally begins with Hermann Muller's classic paper from 1950. It has been extended and refined by him and many others since then (Muller, 1950; Muller, 1966).
An article on Nature: INDEX reports on a recent survey of scientists: Cutting corners a bigger problem than research fraud. The subtitle says it all: Scientists are more concerned about the impact of sloppy science than outright scientific fraud.
The survey was published on BioMed Central.
But to use just one example of advances in philosophical understanding, UofT (specifically Regis College) houses the Lonergan Research Institute, which houses Bernard Lonergan's archives and publishes his collected works. Probably his most significant work is a seven-hundred-page tome called Insight, the first edition of which was published in 1957. It is IMHO the single best account of how humans come to know anything that has ever been written. The tremendous fruits that it has wrought cannot be summarized in a FB commend. Instead, I'd suggest that you walk over and see the friendly people at the LRI. No doubt they could help answer some of your questions.Here's a Wikipedia link to Bernard Lonergan. He was a Canadian Jesuit priest who died in 1984. Regis College is the Jesuit College associated with the University of Toronto.
Note: In my response to Bernier on Facebook I said, "I guess I'll just have to take our word for it. I'm not about to walk over to Regis College and consult a bunch of Jesuit priests about the nature of reality." Was I being too harsh? Is this really an examples of a significant contribution of philosophy? Is it possible that a philosopher could be very wrong about the existence of supernatural beings but still make a contribution to the nature of knowledge and understanding?
1. Jonathan Bernier tells me on Facebook that he is not a philosopher and never claimed to be a philosopher.
Philosophers, historians, and sociologists of science such as Thomas Kuhn, Paul Feyerabend, Bruno Latour, Bas van Fraassen, and Ian Hacking have changed the way that we see the purpose of science in everyday life, as well as proper scientific conduct. Kuhn's concept of a paradigm shift is now so commonplace as to be cliche. Meanwhile, areas like philosophy of physics and especially philosophy of biology are sites of active engagement between philosophers and scientists about the interpretation of scientific results.
[According to Ensembl86] the human genome encodes 58,037 genes, of which approximately one-third are protein-coding (19,950), and yields 198,093 transcripts. By comparison, the mouse genome encodes 48,709 genes, of which half are protein-coding (22,018 genes), and yields 118,925 transcripts overall.The very latest Ensembl estimates (April 2017) for Homo sapiens and Mus musculus are similar. The difference in gene numbers between mouse and human is not significant according to the authors ...
The discrepancy in total number of annotated genes between the two species is unlikely to reflect differences in underlying biology, and can be attributed to the less advanced state of the mouse annotation.This is correct but it doesn't explain the other numbers. There's general agreement on the number of protein-coding genes in mammals. They all have about 20,000 genes. There is no agreement on the number of genes for functional noncoding RNAs. In its latest build, Ensemble says there are 14,727 lncRNA genes, 5,362 genes for small noncoding RNAs, and 2,222 other genes for nocoding RNAs. The total number of non-protein-coding genes is 22,311.
Breschi, A., Gingeras, T.R., and Guigó, R. (2017) Comparative transcriptomics in human and mouse. Nature Reviews Genetics [doi: 10.1038/nrg.2017.19]
Breschi, A., Gingeras, T. R., and Guigó, R. (2017). Comparative transcriptomics in human and mouse. Nature Reviews Genetics [doi: 10.1038/nrg.2017.19]I was confused by the comments made by the authors when they started comparing the human and mouse genomes. They said,
Cross-species comparisons of genomes, transcriptomes and gene regulation are now feasible at unprecedented resolution and throughput, enabling the comparison of human and mouse biology at the molecular level. Insights have been gained into the degree of conservation between human and mouse at the level of not only gene expression but also epigenetics and inter-individual variation. However, a number of limitations exist, including incomplete transcriptome characterization and difficulties in identifying orthologous phenotypes and cell types, which are beginning to be addressed by emerging technologies. Ultimately, these comparisons will help to identify the conditions under which the mouse is a suitable model of human physiology and disease, and optimize the use of animal models.
The most recent genome assemblies (GRC38) include 3.1 Gb and 2.7 Gb for human and mouse respectively, with the mouse genome being 12% smaller than the human one.I think this statement is misleading. The size of the human genome isn't known with precision but the best estimate is 3.2 Gb [How Big Is the Human Genome?]. The current "golden path length" according to Ensembl is 3,096,649,726 bp. [Human assembly and gene annotation]. It's not at all clear what this means and I've found it almost impossible to find out; however, I think it approximates the total amount of sequenced DNA in the latest assembly plus an estimate of the size of some of the gaps.
[Image Credit: Wikipedia: Creative Commons Attribution 2.0 Generic license]
In Debating alternative splicing (Part III) I discussed a review published in the February 2017 issue of Trends in Biochemical Sciences. The review examined the data on detecting predicted protein isoforms and concluded that there was little evidence they existed.
My colleague at the University of Toronto, Ben Blencowe, is a forceful proponent of massive alternative splicing. He responded in a letter published in the June 2017 issue of Trends in Biochemical Sciences (Blencowe, 2017). It's worth looking at his letter in order to understand the position of alternative splicing proponents. He begins by saying,It is estimated that approximately 95% of multiexonic human genes give rise to transcripts containing more than 100 000 distinct AS events [3,4]. The majority of these AS events display tissue-dependent variation and 10–30% are subject to pronounced cell, tissue, or condition-specific regulation [4].
I recently had a chance to talk science with my old friend and colleague Jack Greenblatt. He has recently teamed up with some of my other colleagues at the University of Toronto to publish a paper on alternative splicing in mouse cells. Over the years I have had numerous discussions with these colleagues since they are proponents of massive alternative splicing in mammals. I think most splice variants are due to splicing errors.
There's always a problem with terminology whenever we get involved in this debate. My position is that it's easy to detect splice variants but they should be called "splice variants" until it has been firmly established that the variants have a biological function. This is not a distinction that's acceptable to proponents of massive alternative splicing. They use the term "alternative splicing" to refer to any set of processing variants regardless of whether they are splicing errors or real examples of regulation. This sometimes makes it difficult to have a discussion.
The ongoing debate over junk DNA often revolves around data collected by ENCODE and others. The idea that most of our genome is transcribed (pervasive transcription) seems to indicate that genes occupy most of the genome. The opposing view is that most of these transcripts are accidental products of spurious transcription. We see the same opposing views when it comes to transcription factor binding sites. ENCODE and their supporters have mapped millions of binding sites throughout the genome and they believe this represent abundant and exquisite regulation. The opposing view is that most of these binding sites are spurious and non-functional.
The messy view is supported by many studies on the biophysical properties of transcription factor binding. These studies show that any DNA binding protein has a low affinity for random sequence DNA. They will also bind with much higher affinity to sequences that resemble, but do not precisely match, the specific binding site [How RNA Polymerase Binds to DNA; DNA Binding Proteins]. If you take a species with a large genome, like us, then a typical DNA protein binding site of 6 bp will be present, by chance alone, at 800,000 sites. Not all of those sites will be bound by the transcription factor in vivo because some of the DNA will be tightly wrapped up in dense chromatin domains. Nevertheless, an appreciable percentage of the genome will be available for binding so that typical ENCODE assays detect thousand of binding sites for each transcription factor.Watch this video. It dates from this year. Almost everything Wells says is either false or misleading. Why? Is he incapable of learning about genomes, junk DNA, and evolutionary theory?
Most of the human genome is transcribed at some time or another in some tissue or another. The phenomenon is now known as pervasive transcription. Scientists have known about it for almost half a century.
At first the phenomenon seemed really puzzling since it was known that coding regions accounted for less than 1% of the genome and genetic load arguments suggested that only a small percentage of the genome could be functional. It was also known that more than half the genome consists of repetitive sequences that we now know are bits and pieces of defective transposons. It seemed unlikely back then that transcripts of defective transposons could be functional.New genes can arise by gene duplication. These events are quite common on an evolutionary time scale. In the current human population, for example, there are about 100 examples of polymorphic gene duplications. These are cases where some of us have two copies of a gene while others have only one copy (Zarrie et al., 2015). Humans have gained about 700 new genes by duplication and fixation since we diverged from chimpanzees (Demuth et al., 2006). The average rate of duplication in eukaryotes is about 0.01 events per gene per million years and the half-life of a duplicated gene is about 4 million years (Lynch and Conery, 2003).
The typical fate of these duplicated genes is to "die" by mutation or deletion. There are five possible fates [see Birth and death of genes in a hybrid frog genome]:
When the technology enabling the study of molecular polymorphisms—variations in the sequences of genes and proteins—first arose, a great deal more variability was discovered in natural populations than most evolutionary biologists had expected under natural selection. The neutral theory made the bold claim that these polymorphisms become prevalent through chance alone. It sees polymorphism and long-term evolutionary change as two aspects of the same phenomenon: random changes in the frequencies of alleles. While the neutral theory does not deny that natural selection may be important in adaptive evolutionary change, it does claim that natural selection accounts for a very small fraction of genetic evolution.I don't think there's any doubt that this claim is correct as long as you stick to the proper definition of evolution. The vast majority of fixations of alleles are likely due to random genetic drift and not natural selection.
A dramatic consequence now follows. Most evolutionary change at the genetic level is not adaptive.
It is difficult to imagine random changes accomplishing so much. But random genetic drift is now widely recognized as one of the most important mechanisms of evolution.
Originally proposed by Motoo Kimura, Jack King, and Thomas Jukes, the neutral theory of molecular evolution is inherently non-Darwinian. Darwinism asserts that natural selection is the driving force of evolutionary change. It is the claim of the neutral theory, on the other hand, that the majority of evolutionary change is due to chance.I would just add that it's Neutral Theory PLUS the other effects of random genetic drift that make evolution much more random than most people believe.
In 2013, the ENCODE (Encyclopedia of DNA Elements) Project published results suggesting that eighty per cent of the human genome serves some function. This was considered a rebuttal to the widely held view that a large part of the genome was junk, debris collected over the course of evolution. Hughes sided with his friend Dan Graur in rejecting this point of view. Their argument was simple. Only ten per cent of the human genome shows signs of purifying selection, as opposed to neutrality.
