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In percentage, how much is the human genome (DNA) similar to the mouse genome?


Some guy argued with me against evolution theory, and he claimed that human and mice share 98% just like human and chimpanzee.
I've tried to search online for a simple and accurate answer, but I couldn't yet.
In simple words, how much is the human genome (DNA) similar to the mouse genome?

Please use numbers as much as you can and provide references.


This question cannot be answered as simply as you put it, but it's not too much to elaborate on.

The order of the base pairs will be drastically different, but the same proteins and amino acids will be coded for in genes, just at different points along the DNA. For example, you may find the same sequence to code for a protein in a mouse as in a human, but they will not be found in the same place along the DNA code (although they will still be read and eventually produce the same protein).

http://www.nature.com/nature/journal/v420/n6915/full/nature01262.html Additionally, this article shows that, if we take your question literally, "at the nucleotide level, approximately 40% of the human genome can be aligned to the mouse genome", that is, if human and mouse DNA was lined up side-by-side, and a percentage of identical match-ups was calculated.

However, taking a 'looser' approach, it is worth noting that about 5 percent of both of genomes consist of protein-coding genes (https://www.genome.gov/10001345), and the remaining 90%+ is non-coding. If we only count the protein-coding genes, the average similarity of genes between humans and mice in only protein-coding genes is 85%. The link above says that some are 99%, and some are 60% - there is a clear similarity here between humans and mice, albeit not 100% identical.

If you wish to know the explanation, simply it is because mice and humans both have a common ancestor (the last link also explains this) about 80 million years ago. Due to these similarities, and the striking similarities, scientists simulate genetic changes in mice that can occur to humans, and have used computers to analyse the similarities in mouse genome.

I hope this is understandable, if you need any clarification on terms, please ask :)


How similar are human and chimpanzee genomes?

I recently participated in a discussion on the Biologos forum on the degree of similarity between the human and chimpanzee genomes. I was asked for my current view on this issue by Dennis Venema, who had found a old quote online from a newspaper article that I had written in 2008 on this issue. In 2008, in a couple of newspaper articles, I did some simple calculations based on the 2005 Chimpanzee genome paper. On the basis of these, I had come to the surprising conclusion that these data suggested that the human and chimpanzee genomes in their entirety could be only 70% identical. Dennis Venema asked me if this was still my view. You can read the whole discussion here. It is rather long, with lots of tangential contributions. If you want a quick summary of my perspective, here is my final closing statement (which I originally posted here):

“How similar are the human and chimpanzee genomes?” is a relatively straightforward scientific question. We are hindered by the still somewhat incomplete nature of both the human and the chimpanzee reference genome assemblies, but we can make this clear in our assessments and allow for the uncertainties that it raises.

The best way to assess the similarity of two genomes is to take complete genome assemblies of both species, that have been assembled independently, and align them together. The alignment process involves searching the contents of the two genomes against each other. Parts of both genomes that are too different to match one another will be absent from the alignment, unless they are very short, in which case they will be included as “indels” (longer indels, even if they have well characterised flanking sequences, will be absent from the alignment). Within parts that do align, there will be some mismatches between the two genomes, where one or a few nucleotides differ, which in this discussion we have been calling “SNPs”. In addition there will be some parts of each genome that are present twice or multiple times in one genome and are present fewer times in the other genome. We have referred to these as “paralogs” or “copy number variants” (CNVs). To come up with an accurate figure of the similarity of the entirety of two genomes, we need to take into account all these types of difference.

For some purposes, when talking about the similarity between two genomes we may want to just focus on one type of difference, such as SNPs. If we do this, we should always specify which types of difference we have and have not taken into account. The most well-known estimates for the similarity of the human and chimpanzee genomes only take into account SNPs and small indels. Copy number variants are less often included, and regions of the two genomes that do not align are commonly ignored.

When assessing the total similarity of the human genome to the chimp genome, we also need to bear in mind that roughly 5% of the human genome has not been fully assembled yet, so the best we can do for that 5% is predict how similar it will be to the chimpanzee genome. We do not yet know for sure. The chimpanzee genome assembly is less well assembled, so in future we may assemble parts of the chimpanzee genome that are similar to the human genome – this is another source of uncertainty to keep in mind.

To come up with the most accurate current assessment that I could of the similarity of the human and chimpanzee genome, I downloaded from the UCSC genomics website the latest alignments (made using the LASTZ software) between the human and chimpanzee genome assemblies, hg38 and pantro6. See discussion post #35 for details. This gave the following for the human genome:

4.06% had no alignment to the chimp assembly
5.18% was in CNVs relative to chimp
1.12% differed due to SNPs in the one-to-one best aligned regions
0.28% differed due to indels within the one-to-one best aligned regions

The percentage of nucleotides in the human genome that had one-to-one exact matches in the chimpanzee genome was 84.38%

In order to assess how improvements in genome assemblies can change these figures, I did the same analyses on the alignment of the older PanTro4 assembly against Hg38 (see discussion post #40). The Pantro4 assembly was based on a much smaller amount of sequencing than the Pantro6 assembly (see discussion post #39). In this Pantro4 alignment:

6.29% had no alignment to the chimp assembly
5.01% was in CNVs relative to chimp
1.11% differed due to SNPs in the one-to-one best aligned regions
0.28% differed due to indels within the one-to-one best aligned regions

The percentage of nucleotides in the human genome that had one-to-one exact matches in the chimpanzee genome was 82.34%.

Thus the large improvement in the chimpanzee genome assembly between PanTro4 and PanTro6 has led to an increase in CNVs detected, and a decrease in the non-aligning regions. It has only increased the one-to-one exact matches from 82.34% to 84.38% even though the chimpanzee genome assembly is at least 8% more complete (I think) in PanTro6.

The PanTro4 assembly has also been aligned to the human genome using the software Mummer 4 (reported in: Marçais, Guillaume, et al. “MUMmer4: A fast and versatile genome alignment system.” PLoS Computational Biology 14.1 (2018): e1005944). This method gives broadly similar figures to my analyses of the UCSC LASTZ alignments. MUMmer places 2.782 Gb of the sequence in mutual best alignments, and the total length of the LASTZ alignment is 2.761Gb. In the MUMmer analysis approximately 306 Mb (9.91%) of the human sequence did not align to the chimpanzee sequence in mutual best alignments. This fits well with the LASTZ result of 6.29% non-aligning plus 5.01% CNV = 11.30% not aligning. Overall, the MUMer software has been slightly more generous in aligning the human and chimp genomes, but as Steve Schaffner has pointed out [here], MUMer is giving a higher estimate of SNP differences within its alignments. This is probably a signal that it has over-aligned the two genomes and some of its alignments are spurious. Thus I think we are best off trusting the LASTZ alignment over the MUMer alignment, though the difference between the results of the two methods is rather small.

As 5% of the human genome is still unassembled, and 5% seems to be CNVs relative to chimp, and 4% is unaligned to the chimp genome, I cannot agree with Dennis Venema [here] and Steve Schaffner [here] that “95% is the best estimate we have for the genome-wide identity of chimps and humans”. I would accept 95% as a prediction, but not as a statement of established fact.

I predict that the 95% figure will prove to be wrong, because (on the basis of my comparison of the PanTro4 and PanTro6 alignments to Hg38) I think that the CNV differences are here to stay, and I doubt that all of the currently unaligned or unsequenced regions of the human genome will prove to all be 95% the same as the chimpanzee genome. Some of the “unaligned” human sequences are medium-sized indels, and it is hard to see why they would not have been assembled in the chimp if they were present. I also expect at least some of these unaligned or unsequenced sequences to be rapidly evolving.

In 2008 I wrote “I predict that when we have a reliable, complete chimpanzee genome, the overall similarity of the human genome will prove to be close to 70% (and very far from 99%).” This prediction is not borne out by the more recent data above. I made a mistake in my 2008 calculations in the way in which I dealt with CNVs, which put me out by 2.7%, but this was only a minor component of why my estimate was so low. The main reason why my estimate was so low was because I thought that the 2005 chimpanzee genome assembly was far more complete than it actually was. This was because the authors claimed in the main text of the chimpanzee paper “the draft genome assembly…covers

94% of the chimpanzee genome with >98% of the sequence in high-quality bases.” Thanks to discussion in this thread with Steve Schaffner (see post #62, #63 and others in the discussion), who was one of the authors of the 2005 chimp genome paper, I can now see that the 2005 draft genome assembly was not as good as this claim suggested. However, in 2008 I did not know this, and my prediction was made in good faith on the basis of my understanding of the 2005 paper.


Mouse And Human Genome Remarkably Similar, Despite Differences In Immune System

Mice have been used for scientific study since the 16th century, when William Harvey wanted to learn more about reproduction and blood circulation. Even after hundreds of years of technological innovation, the ordinary lab mouse is still the go-to option for learning more about our own species — and for good reason.

A large international consortium study recently found humans and mice have a lot in common in terms of how our genes are expressed and regulated. While mice don’t hold a candle to the genetic similarities of, say, the chimpanzee, whose genes are 96 percent similar to our own, the majority of the mouse’s genes that have endured through evolution are indeed “conserved” — meaning they serve the same functions after all these years — just as humans’ are.

“This is the first systematic comparison of the mouse and human at the genomic level,” said Dr. Bing Ren, a professor of cellular and molecular medicine at the University of California, San Diego, and a co-senior author of the new study, in a statement. Ren and an enormous team of colleagues from around the world found many of the processes and pathways are shared between humans and mice. “This allows us to study human disease by studying those aspects of mouse biology that reflect human biology,” he said.

Some differences were bound to show up. Immune system processes and some related to metabolism and stress response tended to differ in mice. That doesn’t mean, however, that scientists should be throwing out their studies on genes related to immune function and metabolism just because they used mouse models as their vehicle for investigation.

“That’s not the message we want to convey,” Dr. Feng Yue, first author of the study and Penn State University professor in the Department of Biochemistry and Molecular Biology, told Medical Daily. “We want to say that, indeed, mice are probably the best system to use for studying these two systems. But if you’re studying the immune system using mouse models you probably need to be more careful and perform more functional experiments. It’s not saying that their findings are wrong.”

The findings come on the heels of the ongoing mouse version of ENCODE — the Encyclopedia of DNA Elements — a parts list of the entire mouse genome that launched in 2007 as a way to complement the existing human ENCODE, which was published in full in 2012. In the latest study, researchers analyzed 100 different mouse cell types and tissues. They found many of the underlying processes (genomic functions) served the same purpose, but the mechanisms that let those things happen were different.

“In general, the gene regulation machinery and networks are conserved in mouse and human, but the details differ quite a bit,” said co-senior author Dr. Michael Snyder, director of the Stanford Center for Genomics and Personalized Medicine. But even though they may differ, what scientists care about is how they’re expressed. The trick is not getting lost in translation. “By understanding the differences,” Snyder added, “we can understand how and when the mouse model can best be used.”

That perhaps is the crucial point going forward. While mice models have been researched time and again for their differences to human models, scientists had yet to understand how they are different or how much they are different. Now they can use these important differences to pinpoint where similarities actually lie.

“By the most comprehensive studies,” Yue said, “we confirm it is, indeed, a good system to use.”


New Research Suggests at Least 75% of The Human Genome Is Junk DNA After All

At least three quarters of the human genome consists of non-functional, 'junk DNA', according to a new study, and the actual proportion is likely to be even greater than that.

Ever since Watson and Crick discovered the double helix structure of DNA back in the 1950s, scientists have been debating what extent of the genome is responsible for making you you – and now an evolutionary biologist says the answer to the riddle lies in some basic math.

Dan Graur from the University of Houston calculates that the functional portion of the human genome probably constitutes only about 10 to 15 percent of our overall DNA, with an upper limit of 25 percent.

The rest of our genome – somewhere between around 75 to 90 percent of our DNA – is what's called junk DNA: not necessarily harmful or toxic genetic matter, but useless, garbled nucleotide sequences that aren't functional in terms of encoding proteins that spur all the important chemical reactions going off inside our bodies.

The rationale for Graur's model is based on the way mutations creep into DNA, and how as a species we weed these mutations out for the benefit of all.

These kinds of genetic variants, called deleterious mutations, appear in our genome over time, subtly shifting or reordering the four chemical bases that make up DNA – adenine, cytosine, guanine and thymine – in parts of our genetic code.

When mutations take place in junk DNA, they're considered neutral – since that genetic code doesn't do anything, anyway – but when mutations occur to our functional, defining DNA, they can often be harmful and even ultimately lethal, as they mess up the instructions that code for healthy tissue and biological processes.

On that basis, it's better for our evolutionary prospects if less of our DNA is functional, because less of it is then exposed to the risk of mutation and the increased chances of early death it invites.

In Graur's calculations, given the risk of deleterious mutations to the survival of the species on one hand – and the known stability of population and reproduction rates throughout human history on the other – the limit of functional DNA has to be very low.

Otherwise dangerous mutations would keep stacking up, meaning we'd have to produce impossibly huge numbers of offspring for the small percentage of healthy bubs to survive.

"Under the assumption of 100 percent functionality and the range of deleterious mutation rates used in this paper, maintaining a constant population size would necessitate that each couple on average produce a minimum of 24 and a maximum of 5 × 10 53 children," he writes in his paper.

Of course, nobody really other than creationists is suggesting that we carry around zero junk DNA, but a huge 2012 study called the Encyclopaedia of DNA Elements (ENCODE) project did claim that as much as 80 percent of human DNA was functional.

That study was controversial – partly because many scientists claimed that the ENCODE definition of 'functional' was too broad.

In Graur's use of the term – where functional DNA is code that's evolved to be useful in terms of its evolutionary effects – the 80 percent figure just doesn't add up.

"For 80 percent of the human genome to be functional, each couple in the world would have to beget on average 15 children and all but two would have to die or fail to reproduce," he writes.

It's more likely then that only about 10 to 25 percent isn't junk DNA, Graur thinks.

While his is unlikely to be the last word on the subject – the new results do coincide somewhat neatly with the findings of a separate 2014 study – and could help focus vital scientific efforts on researching a smaller window of uncontested, 'functional' DNA.

"We need to know the functional fraction of the human genome in order to focus biomedical research on the parts that can be used to prevent and cure disease," Graur says.

"There is no need to sequence everything under the sun. We need only to sequence the sections we know are functional."


New Genome Comparison Finds Chimps, Humans Very Similar At DNA Level

WASHINGTON, Wed., Aug. 31, 2005 -- The first comprehensive comparisonof the genetic blueprints of humans and chimpanzees shows our closestliving relatives share perfect identity with 96 percent of our DNAsequence, an international research consortium reported today.

In a paper published in the Sept. 1 issue of the journal Nature, theChimpanzee Sequencing and Analysis Consortium, which is supported inpart by the National Human Genome Research Institute (NHGRI), one ofthe National Institutes of Health (NIH), describes its landmarkanalysis comparing the genome of the chimp (Pan troglodytes) with thatof human (Homo sapiens).

"The sequencing of the chimp genome is a historic achievementthat is destined to lead to many more exciting discoveries withimplications for human health," said NHGRI Director Francis S. Collins,M.D., Ph.D. "As we build upon the foundation laid by the Human GenomeProject, it's become clear that comparing the human genome with thegenomes of other organisms is an enormously powerful tool forunderstanding our own biology."

The chimp sequence draft represents the first non-humanprimate genome and the fourth mammalian genome described in a majorscientific publication. A draft of the human genome sequence waspublished in February 2001, a draft of the mouse genome sequence waspublished in December 2002 and a draft of the rat sequence waspublished in March 2004. The essentially complete human sequence waspublished in October 2004.

"As our closest living evolutionary relatives, chimpanzees areespecially suited to teach us about ourselves," said the study's seniorauthor, Robert Waterston, M.D., Ph.D., chair of the Department ofGenome Sciences of the University of Washington School of Medicine inSeattle. "We still do not have in our hands the answer to a mostfundamental question: What makes us human? But this genomic comparisondramatically narrows the search for the key biological differencesbetween the species."

The 67 researchers who took part in the Chimp Sequencing andAnalysis Consortium share authorship of the Nature paper. Most of thework of sequencing and assembling the chimp genome was done at theBroad Institute of the Massachusetts Institute of Technology andHarvard University, Cambridge, Mass., and the Washington UniversitySchool of Medicine in Saint Louis. In addition to those centers, theconsortium included researchers from institutions elsewhere in theUnited States, as well as Israel, Italy, Germany and Spain.

The DNA used to sequence the chimp genome came from the bloodof a male chimpanzee named Clint at theYerkes National Primate ResearchCenter in Atlanta. Clint died last year from heart failure at therelatively young age of 24, but two cell lines from the primate havebeen preserved at the Coriell Institute for Medical Research in Camden,N.J.

The consortium found that the chimp and human genomes are verysimilar and encode very similar proteins. The DNA sequence that can bedirectly compared between the two genomes is almost 99 percentidentical. When DNA insertions and deletions are taken into account,humans and chimps still share 96 percent of their sequence. At theprotein level, 29 percent of genes code for the same amino sequences inchimps and humans. In fact, the typical human protein has accumulatedjust one unique change since chimps and humans diverged from a commonancestor about 6 million years ago.

To put this into perspective, the number of geneticdifferences between humans and chimps is approximately 60 times lessthan that seen between human and mouse and about 10 times less thanbetween the mouse and rat. On the other hand, the number of geneticdifferences between a human and a chimp is about 10 times more thanbetween any two humans.

The researchers discovered that a few classes of genes arechanging unusually quickly in both humans and chimpanzees compared withother mammals. These classes include genes involved in perception ofsound, transmission of nerve signals, production of sperm and cellulartransport of electrically charged molecules called ions. Researcherssuspect the rapid evolution of these genes may have contributed to thespecial characteristics of primates, but further studies are needed toexplore the possibilities.

The genomic analyses also showed that humans and chimps appearto have accumulated more potentially deleterious mutations in theirgenomes over the course of evolution than have mice, rats and otherrodents. While such mutations can cause diseases that may erode aspecies' overall fitness, they may have also made primates moreadaptable to rapid environmental changes and enabled them to achieveunique evolutionary adaptations, researchers said.

Despite the many similarities found between human and chimpgenomes, the researchers emphasized that important differences existbetween the two species. About 35 million DNA base pairs differ betweenthe shared portions of the two genomes, each of which, like mostmammalian genomes, contains about 3 billion base pairs. In addition,there are another 5 million sites that differ because of an insertionor deletion in one of the lineages, along with a much smaller number ofchromosomal rearrangements. Most of these differences lie in what isbelieved to be DNA of little or no function. However, as many as 3million of the differences may lie in crucial protein-coding genes orother functional areas of the genome.

"As the sequences of other mammals and primates emerge in thenext couple of years, we will be able to determine what DNA sequencechanges are specific to the human lineage. The genetic changes thatdistinguish humans from chimps will likely be a very small fraction ofthis set," said the study's lead author, Tarjei S. Mikkelsen of theBroad Institute of MIT and Harvard. Among the genetic changes thatresearchers will be looking for are those that may be related to thehuman-specific features of walking upright on two feet, a greatlyenlarged brain and complex language skills.

Although the statistical signals are relatively weak, a fewclasses of genes appear to be evolving more rapidly in humans than inchimps. The single strongest outlier involves genes that code fortranscription factors, which are molecules that regulate the activityof other genes and that play key roles in embryonic development.

A small number of other genes have undergone even moredramatic changes. More than 50 genes present in the human genome aremissing or partially deleted from the chimp genome. The correspondingnumber of gene deletions in the human genome is not yet preciselyknown. For genes with known functions, potential implications of thesechanges can already be discerned.

For example, the researchers found that three key genesinvolved in inflammation appear to be deleted in the chimp genome,possibly explaining some of the known differences between chimps andhumans in respect to immune and inflammatory response. On the otherhand, humans appear to have lost the function of the caspase-12 gene,which produces an enzyme that may help protect other animals againstAlzheimer's disease.

"This represents just the tip of the iceberg when it comes toexploring the genomic roots of our biological differences," said one ofthe study's co-authors LaDeana W. Hillier of the Genome SequencingCenter at Washington University School of Medicine. "As more is learnedabout other functional elements of the genome, we anticipate that otherimportant differences outside of the protein-coding genes will emerge."

Armed with the chimp sequence, researchers also scanned theentire human genome for deviations from normal mutation patterns. Suchdeviations may reveal regions of "selective sweeps," which occur when amutation arises in a population and is so advantageous that it spreadsthroughout the population within a few hundred generations andeventually becomes "normal."

The researchers found six regions in the human genome that havestrong signatures of selective sweeps over the past 250,000 years. Oneregion contains more than 50 genes, while another contains no knowngenes and lies in an area that scientists refer to as a "gene desert."Intriguingly, this gene desert may contain elements regulating theexpression of a nearby protocadherin gene, which has been implicated inpatterning of the nervous system. A seventh region with moderatelystrong signals contains the FOXP2 and CFTR genes. FOXP2 has beenimplicated in the acquisition of speech in humans. CFTR, which codesfor a protein involved in ion transport and, if mutated, can cause thefatal disease cystic fibrosis, is thought to be the target of positiveselection in European populations.


Laboratory Rat Gene Sequencing Completed Humans Share One-fourth Of Genes With Rat, Mouse

A large team of researchers, including a computer scientist at Washington University in St. Louis, has effectively completed the genome sequence of the common laboratory brown rat, Rattus norvegicus. This makes the third mammal to be sequenced, following the human and mouse.

The Rat Genome Sequencing Project Consortium (RGSPC), led by the Human Genome Sequencing Center at Baylor College of Medicine (BCM-HGSC) in Houston, in conjunction with the National Heart, Lung and Blood Institute (NHLBI) and the National Human Genome Research Institute (NHGRI), announced today the generation and analysis of the genome sequence of the Brown Norway (BN) rat. The high quality 'draft' sequence covers over 90 percent of the genome. The primary results are presented in the April 1 issue of Nature, and an additional thirty manuscripts describing further detailed analyses are contained in the April issue of Genome Research.

"This is an investment that is destined to yield major payoffs in the fight against human disease," said NIH Director Elias A. Zerhouni, M.D. "For nearly 200 years, the laboratory rat has played a valuable role in efforts to understand human biology and to develop new and better drugs. Now, armed with this sequencing data, a new generation of researchers will be able to greatly improve the utility of rat models and thereby improve human health."

The laboratory rat is an indispensable tool in experimental medicine and drug development and has made inestimable contributions to human health. The new data expand and consolidate its role as a research resource. The BN rat sequence is the third complete mammalian genome to be sequenced to high quality and described in a major scientific publication. Three-way comparisons with the human and mouse genomes will help to resolve details of mammalian evolution.

"The sequencing of the rat genome constitutes another major milestone in our effort to expand our knowledge of the human genome," said NHGRI Director Francis S. Collins, M.D., Ph.D. "As we build upon the foundation laid by the Human Genome Project, it's become clear that comparing the human genome with those of other organisms is the most powerful tool available to understand the complex genomic components involved in human health and disease."

Michael R. Brent, Ph.D., associate professor of computer science and engineering at Washington University in St. Louis, contributed to the analysis of the gene set. According to Brent, results from the study show that the change from the last common ancestor of rodents and humans has occurred much faster along the rodent branch than change along the human branch. Also, the study finds that approximately one-fourth of the human genome is shared with both rats and mice.

That's approximately 700 megabases of DNA shared by all three animals.

"It's surprising that the amount of shared DNA is so small," Brent said.

Relative to their last common ancestor, the rodent lineage has mutated more than the human lineage, Brent pointed out, while analysis of the human genome reveals significantly more segmental duplication &ndash a biological process whereby a large piece of the genome is copied in small numbers. Segmental duplications are one of the key things that differentiate the human genome from that of chimpanzees, and may contribute to the physical and behavioral difference between the two species.

Rodent mutation is due to various different factors, an obvious one being generation time &ndash they reproduce faster than humans. The results of the analysis show that the rat has mutated slightly more frequently than the mouse from the last common ancestor. "It's not clear how to explain that because they both have the same generation time," Brent said.

Results also show there is nearly two times more mutation in the brown rat male germ line than the female germ line, perhaps because there are more cell divisions along the path to making a sperm than the path to making an egg, and thus more chance for error Females carry two X chromosomes and males one. The study finds less mutation in the X chromosome than in chromosomes equally divided between males and females.

A network of centers generated data and resources for the RGSP, including the BCM-HGSC, Celera Genomics, Genome Therapeutics Corporation, British Columbia Cancer Agency Genome Sciences Centre, The Institute for Genomic Research, University of Utah, Medical College of Wisconsin, The Children's Hospital of Oakland Research Institute, and Max-Delbrück-Center for Molecular Medicine (Berlin). After assembly of the genome at the BCM-HGSC, analysis was performed by an international team, representing over 20 groups in six countries and relying largely on gene and protein predictions produced by the Ensembl project of the EMBL-EBI and Sanger Institute (UK). Funding for the RGSP was largely provided by the NHLBI and the NHGRI with additional private funding provided to the BCM-HGSC by the Kleberg Foundation.

The study found the rat genome contains similar numbers of genes to the human and mouse genomes but at 2.75 gigabases (Gb) is smaller than human (2.9 Gb) and slightly larger than mouse (2.6 Gb). Almost all human genes known to be associated with diseases have counterparts in the rat genome and appear highly conserved through mammalian evolution. A selected few families of genes have been expanded in the rat, including smell receptors and genes for dealing with toxins, and these give clues to the distinctive physiology of the species.

Current examples of use of the rat in human medical research include surgery, transplantation, cancer, diabetes, psychiatric disorders including behavioral intervention and addiction, neural regeneration, wound and bone healing, space motion sickness, and cardiovascular disease. In drug development, the rat is routinely employed both to demonstrate therapeutic efficacy and assess toxicity of novel therapeutic compounds prior to human clinical trials. The genome sequence will facilitate all of these studies.

As the third mammalian genome to be completely sequenced, comparison of the rat genome to human and mouse allows a unique view of mammalian evolution. The rat data shows about 40 percent of the modern mammalian genome derives from the last common mammalian ancestor. These 'core' one billion bases encode nearly all the genes and their regulatory signals, accounting for the similarities among mammals. These parts of the genome will be of particular focus in other mammals as new genomes are explored, and the events leading to the current species are unraveled.

"Future work aimed at identifying the genomic differences that contribute to evolution and disease will benefit from analyses such as these, which will become increasingly powerful as the repertoire of mammalian genome sequences expands" said Richard Gibbs, Ph.D., director of the BCM-HGSC and overall principal investigator of the RGSP.

To ensure a high quality draft, the combined approach used both whole genome shotgun (WGS) and BAC clone sequencing techniques. To merge these into the final draft sequence, the BCM-HGSC developed the Atlas software package for genome assembly. The resulting genome sequence was contained in 291 large segments, with a typical length of 19 megabases (Mb). Moreover, the structure of the 3 percent of the genome containing recent duplications, where genes are born, was accurately determined by the Atlas assembler. These statistics match or exceed other draft genome sequences. Overall, the combined approach takes advantage of strengths of previous methods, either pure WGS or pure BAC sequencing, with few of the disadvantages.

"The issue of efficacy of WGS versus other approaches to the sequencing of large genomes remains a matter of earnest scientific debate, and methodology for producing draft sequences continues to evolve" said Dr. George Weinstock, co-director of the BCM-HGSC.

Following the rat project, the BCM-HGSC has undertaken the genomes of the honeybee and sea urchin, and is now working on the Bovine and Rhesus macaque projects. Like the rat, each will lead to a high quality genome draft sequence. With advances in genome technologies it is likely that genomes from many different species can be analyzed in the next three years.


Researchers Compare Chicken, Human Genomes: Analysis Of First Avian Genome Uncovers Differences Between Birds And Mammals

BETHESDA, Md., Wed., Dec. 8, 2004 &ndash An international research consortium has found that chickens and humans share more than half of their genes, but that their DNA sequences diverge in ways that may explain some of the important differences between birds and mammals. The consortium's analysis is published in the Dec. 9 issue of the journal Nature.

The International Chicken Genome Sequencing Consortium analyzed the sequence of the Red Jungle Fowl (Gallus gallus), which is the progenitor of domestic chickens. The National Human Genome Research Institute (NHGRI), part of the National Institutes of Health, provided about $13 million in funding for the project, which involved researchers from China, Denmark, France, Germany, Japan, Poland, Singapore, Spain, Sweden, Switzerland, the United Kingdom and the United States.

The chicken is the first bird, as well as the first agricultural animal, to have its genome sequenced and analyzed. The first draft of the chicken genome, which was based on 6.6-fold coverage, was deposited into free public databases for use by researchers around the globe in March 2004. Over the past nine months, the consortium carefully analyzed the genome and compared it with the genomes of organisms that have already been sequenced, including the human, the mouse, the rat and the puffer fish.

"The chicken genome fills a crucial gap in our scientific knowledge. Located between mammals and fish on the tree of life, the chicken is well positioned to provide us with new insights into genome evolution and human biology," said NHGRI Director Francis S. Collins, M.D., Ph.D. "By comparing the genomes of a wide range of animals, we can better understand the structure and function of human genes and, ultimately, develop new strategies to improve human health."

In their paper published in Nature, members of the International Chicken Genome Sequencing Consortium report that the chicken genome contains significantly less DNA than the human genome, but approximately the same number of genes. Researchers estimate that the chicken has about 20,000-23,000 genes in its 1 billion DNA base pairs, compared with the human count of 20,000-25,000 genes in 2.8 billion DNA base pairs. The difference in total amount of DNA reflects a substantial reduction in DNA repeats and duplications, as well as fewer pseudogenes, in the chicken genome.

About 60 percent of chicken genes correspond to a similar human gene. However, researchers uncovered more small sequence differences between corresponding pairs of chicken and human genes, which are 75 percent identical on average, than between rodent and human gene pairs, which are 88 percent identical on average. Differences between human and chicken genes were not uniform across the board, however. Chicken genes involved in the cell's basic structure and function showed more sequence similarity with human genes than did those implicated in reproduction, immune response and adaptation to the environment.

The analysis also showed that genes conserved between human and chicken often are also conserved in fish. For example, 72 percent of the corresponding pairs of chicken and human genes also possess a counterpart in the genome of the puffer fish (Takifugu rubripes). According to the researchers, these genes are likely to be present in most vertebrates.

"Genomes of the chicken and other species distant from ourselves have provided us with a powerful tool to resolve key biological processes that have been conserved over millennia," said Richard Wilson, Ph.D., of Washington University School of Medicine in St. Louis, the consortium's leader and senior author of the Nature article. "Along with the many similarities between the chicken and human genomes, we discovered some fascinating differences that are shedding new light on what distinguishes birds from mammals."

Like all birds, chickens are thought to have descended from dinosaurs in the middle of the Mesozoic period and have evolved separately from mammals for approximately 310 million years. Chickens were first domesticated in Asia, perhaps as early as 8000 B.C.

As might be expected, genomic researchers determined that chickens have an expanded gene family coding for a type of keratin protein used to produce scales, claws and feathers, while mammalian genomes possess more genes coding for another type of keratin involved in hair formation. Likewise, chickens are missing the genes involved in the production of milk proteins, tooth enamel and the detection of hormonal substances called pheromones, which researchers say may mirror the evolution of the mammary glands and the nose in mammals and the loss of teeth in birds. But other results of the analysis caught even the researchers by surprise.

The analysis showed that a group of genes that code for odor receptor proteins is dramatically expanded in the chicken genome &ndash a finding that appears to contradict the traditional view that birds have a poor sense of smell. And, as it turns out, birds might not have such a great sense of taste. When compared with mammals, chickens have a much smaller family of genes coding for taste receptors, particularly those involved in detecting bitter sensations.

Other intriguing findings from the Nature paper include:

* Alignment of chicken and human genes indicate that approximately 2,000 human genes may actually start at different sites than scientists thought. The discovery of these "true" start sites, which appear to lie inside the previously hypothesized boundaries of the genes, may have implications for the understanding of human disease and the design of new therapies.

* Chicken genes that code for eggshell-specific proteins, such as ovocleidin-116, have mammalian counterparts that play a role in bone calcification. Previously, such genes were not known outside of birds. However, the analysis also showed that, in contrast to chickens, mammals are missing key genes coding for proteins involved in egg production, such as egg whites and yolk storage.

* Chickens have a gene that codes for interleukin-26 (IL-26), a protein involved in immune response. Previously, this immune-related gene was known only in humans. The discovery means that the chicken may now serve as a model organism in which researchers can investigate the function of IL-26.

* Chickens possess genes coding for certain light-dependent enzymes, while mammals have lost those genes. It is thought losses reflect a period in early mammalian history in which mammals were active mainly at night.

* The avian genome contains a gene that codes for an enzyme involved in generating blue color pigments, while mammals are lacking that gene.

Besides providing insights into gene content and evolution of genes, the consortium's analysis offers new perspectives on the evolution of portions of the genome that do not code for proteins. Less than 11 percent of the chicken genome consists of interspersed segments of short, repetitive DNA sequences, compared with 40 to 50 percent of mammalian genomes. With genes comprising another 4 percent of the chicken genome, researchers say that leaves them with no explanation for the function of more than 85 percent of the chicken genome. They hypothesize this genetic "dark matter" may contain previously unrecognized regulatory elements, but also may include ancient DNA repetitive elements that have mutated beyond recognition. Furthermore, researchers said it appears that the 571 non-coding RNA "genes" that they identified in the chicken genome may use different duplication and/or translocation mechanisms than do regular protein-coding genes, opening the door to a whole new realm of scientific inquiry.

In addition to its tremendous value as a resource for comparative genomics, the chicken is widely used in biomedical research. It serves as an important model for vaccine production and the study of embryology and development, as well as for research into the connection between viruses and some types of cancer.

Recent outbreaks of avian flu have accelerated agricultural researchers' interest in learning more about the chicken genome and how genetic variation may play a role in susceptibility of different strains to the disease. The chicken genome sequence will also serve as a resource for researchers seeking to enhance the nutritional value of poultry and egg products. Furthermore, as the first of 9,600 species of birds to have its genome fully sequenced and analyzed, the chicken genome will help to further understanding of avian genomics and biology in general.


How much of our DNA is junk?

The human genome contains around 20,000 genes, that is, the stretches of DNA that encode proteins. But these genes account for only about 1.2 percent of the total genome. The other 98.8 percent is known as noncoding DNA. Dr. T. Ryan Gregory of the University of Guelph in Ontario believes that while some noncoding DNA is essential, most probably does nothing for us at all, and until recently, most biologists agreed with him. Surveying the genome with the best tools at their disposal, they believed that only a small portion of noncoding DNA showed any evidence of having any function.

But in the past few years, the tide has shifted within the field. Recent studies have revealed a wealth of new pieces of noncoding DNA that do seem to be as important to our survival as our more familiar genes. Many of them may encode molecules that help guide our development from a fertilized egg to a healthy adult, for example. If these pieces of noncoding DNA become damaged, we may suffer devastating consequences like brain damage or cancer, depending on what pieces are affected. Large-scale surveys of the genome have led a number of researchers to expect that the human genome will turn out to be even more full of activity than previously thought.

For Gregory and a group of like-minded biologists, this idea is not just preposterous but also perilous, something that could yield bad science. The turn against the notion of junk DNA, they argue, is based on overinterpretations of wispy evidence and a willful ignorance of years of solid research on the genome. They’ve challenged their opponents face to face at scientific meetings. They’ve written detailed critiques in biology journals. They’ve commented on social media. When the N.I.H.’s official Twitter account relayed Collins’s claim about not using the term “junk DNA” anymore, Michael Eisen, a professor at the University of California, Berkeley, tweeted back with a profanity.

Read full, original article: Is Most of Our DNA Garbage?


In percentage, how much is the human genome (DNA) similar to the mouse genome? - Biology

23andMe celebrates genetic diversity but today we’d like to celebrate our genetic similarities — to other organisms. You are no rabbit or chicken (or, if you are, you are a truly impressive rabbit or chicken to be reading this blog). Rather, your DNA contains all the instructions for making you human. All humans have essentially the same set of genes, but you actually share many of these genes with other animals and even plants.


Chimpanzees, our closest living animal cousins share 98% of our human genes, meaning that for 98% of our genes, there is a similar gene in the chimpanzee genome. Even mammals that look quite different from us share a large percentage of our genes small and furry mice share 92% our genes.

See how genetically similar you are to other people using the Compare Genes feature or see how much DNA you share with Neanderthals in your 23andMe account.

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Non-mammals share a smaller, but still appreciable, percentage of our genes. Fruit flies, for instance, have their own version of approximately 44% our human genes. Many of these genes influence growth and structure in both mammals and insects. More distantly related is yeast, the one-celled organism much loved by bakers and brewers alike. Yeast share about a quarter of our genes, many of which are necessary for basic cell functions. Plants, too, share many genes with humans one type of weed was estimated to share 18% of our genes.

DNA is what makes us unique as individuals and as the human species, and yet DNA also illustrates how connected we are to all other living organisms. Now that’s something to celebrate!

The concept for today’s post was suggested by a 23andMe customer. The percentages presented above can be found at the Marian Koshland Science Museum of the National Academy of Science website.


Watch the video: DNA, Chromosomen, Genom des Menschen Zellbiologie Vorlesung 8 + english subtitles (January 2022).