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According to the report published by Grand View Research Clustered Regularly Interspaced Short Palindromic Repeats CRISPR and CRISPR-associated (Cas) genes market is anticipated to reach USD 4.09 billion by 2025.Possibility of rewriting the host DNA through the virtue of Cas9 by introduction of major modifications can be attributed for rising adoption of technology.

Clustered Regularly Interspaced Short Palindromic RepeatsCRISPR and CRISPR-Associated (Cas) Genes Marketis anticipated to reach USD 4.09 billion by 2025, according to a new report by Grand View Research, Inc. This genome editing principle spans almost every industry that involves biological systems. The rising adoption of technology in different areas associated with biotechnology is anticipated to drive industrial growth of the technology substantially in the coming years.

Possibility of rewriting the host DNA through the virtue of Cas9 by introduction of major modifications can be attributed for rising adoption of technology. These modifications include inversion, deletions, knockouts, translocations, and gene replacement.

Moreover, application of the technology as a qualitative as well as quantitative tool in plant genome editing is expected to propel growth. The technique holds the potential for producing plants with mutations linked to other disciplines of science such as disease resistance, biofuel production, synthetic biology, phytoremediation and abiotic stress tolerance.

Combination of clustered regularly interspaced short palindromic repeats and sequencing technology enables high-throughput analysis of gene regulation thereby resulting to enhancement in genomics sector. The aforementioned combination is applicable in the epigenetic study of diseases such as leukaemia.

However, off-target effects associated with the implementation of CRISPR is anticipated to impede growth in the coming years. These effects include improper concentration ratio between Cas9 and single guide RNA that may result into off-target cleavage.

Full research report on CRISPR and CRISPR-Associated (Cas) Genes Market: http://www.grandviewresearch.com/industry-analysis/crispr-associated-cas-genes-market

Further Key Findings from the Report Suggest:

View more reports of this category by Grand View Research at: http://www.grandviewresearch.com/industry/biotechnology

Grand View Research has segmented the CRISPR and Cas Genes market on the basis of product, application, end-use, and region:

CRISPR and Cas Genes Product Outlook (Revenue, USD Million, 2014 2025)

CRISPR and Cas Genes Application Outlook (Revenue, USD Million, 2014 2025)

CRISPR and Cas Genes End-use Outlook (Revenue, USD Million, 2014 2025)

CRISPR and Cas Genes Regional Outlook (Revenue, USD Million, 2014 2025)

Access press release of this research report by Grand View Research: http://www.grandviewresearch.com/press-release/global-crispr-associated-cas-genes-market

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CRISPR And Cas Genes Market Is Anticipated To Drive Industrial ... - satPRnews (press release)

A new method lets researchers quicklyscreen the non-coding DNA of the human genome for links to diseases that are driven by changes in gene regulation.

The technique could revolutionize modern medicines understanding of the genetically inherited risks of developing heart disease, diabetes, cancer, neurological disorders, and others, and lead to new treatments.

Identifying single mutations that cause rare, devastating diseases like muscular dystrophy has become relatively straightforward, says Charles Gersbach, the associate professor of biomedical engineering at Duke University. But more common diseases that run in families often involve lots of genes as well as genetic reactions to environmental factors. Its a much more complicated story, and weve been wanting a way to better understand it. Now weve found a way.

As reported in Nature Biotechnology, the new technique relies on the gene-hacking system called CRISPR/Cas9. Originally discovered as a natural antiviral defense mechanism in bacteria, the system recognizes and homes in on the genetic code of previous intruders and then chops up their DNA. In the past several years, researchers have harnessed this biologic system to precisely cut and paste DNA sequences in living organisms.

In the current study, researchers added molecular machinery that can control gene activity by manipulating the web of biomolecules that determines which genes each cell activates and to what degree.

With the new tool, Gersbach and his colleagues are exploring the 98 percent of our genetic code often referred to as the dark matter of the genome.

Only a small fraction of our genome encodes instructions to make proteins that guide cellular activity, says Tyler Klann, the biomedical engineering graduate student who led the work in Gersbachs lab. But more than 90 percent of the genetic variation in the human population that is associated with common disease falls outside of those genes. We set out to develop a technology to map this part of the genome and understand what it is doing.

The answer, says Klann, lies with promoters and enhancers. Promoters sit directly next to the genes they control. Enhancers, however, which modulate promoters, can be just about anywhere due to the genomes complex 3D geometry, making it difficult to discern what theyre actually doing.

If an enhancer is dialing a promoter up or down by 10 or 20 percent, that could logically explain a small genetic contribution to cardiovascular disease, for example, says Gersbach. With this CRISPR-based system, we can more strongly turn these enhancers on and off to see exactly what effect theyre having on the cell. By developing therapies that more dramatically affect these targets in the right direction, we could have a significant effect on the corresponding disease.

Thats all well and good for exploring the regions of the genome that researchers have already identified as being linked to diseases, but there are potentially millions of sites in the genome with unknown functions. To dive down the dark genome rabbit hole, Gersbach turned to colleagues Greg Crawford, associate professor of pediatrics and medical genetics, and Tim Reddy, assistant professor of bioinformatics and biostatistics. All three professors work in the Duke Center for Genomic and Computational Biology.

Crawford developed a way of determining which sections of DNA are open for business. That is, which sections are not tightly packed away, providing access for interactions with biomachinery such as RNA and proteins. These sites, the researchers reason, are the most likely to be contributing to a cells activity in some way. Reddy has been developing computational tools for interpreting these large genomic data sets.

Over the past decade, Crawford has scanned hundreds of types of cells and tissues affected by various diseases and drugs and come up with a list of more than 2 million potentially important sites in the dark genomeclearly far too many to investigate one at a time.

In the new study, Crawford, Reddy, and Gersbach demonstrate a high-throughput screening method to investigate many of these potentially important genetic sequences in short order. While these initial studies screened hundreds of these sites across millions of base pairs of the genome, the researchers are now working to scale this up 100- to 1,000-fold.

Small molecules can target proteins and RNA interference targets RNA, but we needed something to go in and modulate the non-coding part of the genome, says Crawford. Up until now, we didnt have that.

The method starts by delivering millions of CRISPR systems loaded into viruses, each targeting a different genetic point of interest, to millions of cells in a single dish. After ensuring each cell receives only one virus, the team screens them for changes in their gene expression or cellular functions.

For example, someone researching diabetes could do this with pancreatic cells and watch for changes in insulin production. Those cells that show interesting alterations are then isolated and sequenced to determine which stretch of DNA the CRISPR affected, revealing a new genetic piece of the diabetes puzzle.

The technique is already producing results, identifying previously known genetic regulatory elements while also spotting a few new ones. The results also show it can be used to turn genes either on or off, which is superior to other tools for studying biology that only turn genes off. Different cell types also produced differentbut partially overlappingresults, highlighting the biological complexity in gene regulation and disease that can be interrogated with this technology.

Now that we have this tool, we can go in and annotate the functions of these previously unknown but important stretches of our genome, says Gersbach. With so many places to look, and the ability to do it quickly and robustly, well undoubtedly find new segments that are important for disease, which will provide new avenues for developing therapeutics.

The Thorek Memorial Foundation, the National Institutes of Health, and the National Science Foundation supported the work.

Source: Duke University

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How scientists explore our genome's 'dark matter' - Futurity: Research News

Researchers have developed a method to swiftly screen the non-coding DNA of the human genome for links to diseases that are driven by changes in gene regulation. The technique could revolutionize modern medicines understanding of the genetically inherited risks of developing heart disease, diabetes, cancer, neurological disorders and others, and lead to new treatments.

The study appeared online in Nature Biotechnology on April 3, 2017.

Identifying single mutations that cause rare, devastating diseases like muscular dystrophy has become relatively straightforward, said Charles Gersbach, the Rooney Family Associate Professor of Biomedical Engineering at Duke University. But more common diseases that run in families often involve lots of genes as well as genetic reactions to environmental factors. Its a much more complicated story, and weve been wanting a way to better understand it. Now weve found a way.

The new technique relies on the gene-hacking system called CRISPR/Cas9. Originally discovered as a natural antiviral defense mechanism in bacteria, the system recognizes and homes in on the genetic code of previous intruders and then chops up their DNA. In the past several years, researchers have harnessed this biologic system to precisely cut and paste DNA sequences in living organisms.

In the current study, researchers added molecular machinery that can control gene activity by manipulating the web of biomolecules that determines which genes each cell activates and to what degree.

With the new tool, Gersbach and his colleagues are exploring the 98 percent of our genetic code often referred to as the dark matter of the genome.

Only a small fraction of our genome encodes instructions to make proteins that guide cellular activity, said Tyler Klann, the biomedical engineering graduate student who led the work in Gersbachs lab. But more than 90 percent of the genetic variation in the human population that is associated with common disease falls outside of those genes. We set out to develop a technology to map this part of the genome and understand what it is doing.

The answer, says Klann, lies with promoters and enhancers. Promoters sit directly next to the genes they control. Enhancers, however, which modulate promoters, can be just about anywhere due to the genomes complex 3D geometry, making it difficult to discern what theyre actually doing.

If an enhancer is dialing a promoter up or down by 10 or 20 percent, that could logically explain a small genetic contribution to cardiovascular disease, for example, said Gersbach. With this CRISPR-based system, we can more strongly turn these enhancers on and off to see exactly what effect theyre having on the cell. By developing therapies that more dramatically affect these targets in the right direction, we could have a significant effect on the corresponding disease.

Thats all well and good for exploring the regions of the genome that researchers have already identified as being linked to diseases, but there are potentially millions of sites in the genome with unknown functions. To dive down the dark genome rabbit hole, Gersbach turned to colleagues Greg Crawford, associate professor of pediatrics and medical genetics, and Tim Reddy, assistant professor of bioinformatics and biostatistics. All three professors work together in the Duke Center for Genomic and Computational Biology.

Crawford developed a way of determining which sections of DNA are open for business. That is, which sections are not tightly packed away, providing access for interactions with biomachinery such as RNA and proteins. These sites, the researchers reason, are the most likely to be contributing to a cells activity in some way. Reddy has been developing computational tools for interpreting these large genomic data sets.

Over the past decade, Crawford has scanned hundreds of types of cells and tissues affected by various diseases and drugs and come up with a list of more than 2 million potentially important sites in the dark genomeclearly far too many to investigate one at a time. In the new study, Crawford, Reddy and Gersbach demonstrate a high-throughput screening method to investigate many of these potentially important genetic sequences in short order. While these initial studies screened hundreds of these sites across millions of base pairs of the genome, the researchers are now working to scale this up 100- to 1000-fold.

Small molecules can target proteins and RNA interference targets RNA, but we needed something to go in and modulate the non-coding part of the genome, said Crawford. Up until now, we didnt have that.

The method starts by delivering millions of CRISPR systems loaded into viruses, each targeting a different genetic point of interest, to millions of cells in a single dish. After ensuring each cell receives only one virus, the team screens them for changes in their gene expression or cellular functions.

For example, someone researching diabetes could do this with pancreatic cells and watch for changes in insulin production. Those cells that show interesting alterations are then isolated and sequenced to determine which stretch of DNA the CRISPR affected, revealing a new genetic piece of the diabetes puzzle.

The technique is already producing results, identifying previously known genetic regulatory elements while also spotting a few new ones. The results also showed it can be used to turn genes either on or off, which is superior to other tools for studying biology which only turn genes off. Different cell types also produced differentbut partially overlappingresults, highlighting the biological complexity in gene regulation and disease that can be interrogated with this technology.

Now that we have this tool, we can go in and annotate the functions of these previously unknown but important stretches of our genome, said Gersbach. With so many places to look, and the ability to do it quickly and robustly, well undoubtedly find new segments that are important for disease, which will provide new avenues for developing therapeutics.

This work was supported by the Thorek Memorial Foundation, the National Institutes of Health (R01DA036865, U01HG007900, DP2OD008586, P30AR066527, T32GM008555, R41GM119914) and the National Science Foundation (CBET-1151035).

CRISPRCas9 epigenome editing enables high-throughput screening for functional regulatory elements in the human genome. Tyler S. Klann, Joshua B. Black, Malathi Chellappan, Alexias Safi, Lingyun Song, Isaac B. Hilton, Gregory E. Crawford, Timothy E. Reddy and Charles A. Gersbach. Nature Biotechnology, April 3, 2017. DOI: 10.1038/nbt.3853

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Screening the Human Genome's 'Dark Matter' - Duke Today

Schultz, et. al., Science

Viruses tend to have stripped-down genomes, carrying just enough genes to take over a cell and make lots more copies. Ebola, for example, carries a total of just seven genes, allowing new copies to be made with little fuss. There are a few exceptionsviruses like herpes with complex life cyclesbut even the biggest of the viruses we knew about had only a few hundred genes.

All that changed a bit more than a decade ago, when researchers discovered the Mimivirus, which had a genome bigger than some bacteria and carried many genes for functions that are normally provided by host proteins. The huge genomes and strange behavior of the viruses led their discoverers to propose that they weren't just odd offshoots that preyed upon liferather, they might have played a critical role in boosting life's complexity.

Now, researchers have discovered a new family of giant viruses, related to the Mimiviruses but distinct in a number of ways. And a careful analysis of their genes suggests they, and all other giant viruses, have been put together through relatively recent evolution. The work argues very strongly against these viruses playing a key role in life's diversification.

The Mimiviruses contain many of the genes needed to read DNA and use the information to make proteins; most other viruses rely entirely on the system that their host cells use. They also set up an odd "virus factory" inside cells they infect, which appears physically distinct from the rest of the cell's contents.

To the people that discovered the virus, this looked almost as if the virus were setting up its own nucleus, the place where cells normally store their DNA. So they suggested this might be how cells ended up with a nucleus in the first place: a virus set up shop in what had been a simple cell, and never left. Additional complexity evolved over time, but many of the virus' genes are still around in complex cells like our own.

While intriguing, the proposal rested on the idea that the giant viruses are a distinct lineage that has been around since the main branches of the tree of life first started. And, from a genetic standpoint, this seemed plausible; many of the genes the viruses carry were either previously unknown or not closely related to the genes of the host they preyed upon.

That idea was put to a test by the combination of an Austrian-US research collaboration and a sewage plant. Samples from the wastewater treatment plant at Klosterneuburg, Austria were subjected to what's called metagenome analysis. Rather than trying to culture everything that grew in the waste, the authors simply isolated DNA from it and started sequencing. Computers can then search for pieces that overlap, gradually building up individual genomes out of the random parts.

This turned up Klosneuvirus, another giant virus with a genome 1.6 million base pairs long. Electron microscopy of the sewage water then revealed giant viruses were present. Struck by this success, the authors then started searching through other metagenome data sets. This search put together three additional giant virus genomes, belonging to Catovirus, Hokovirus, and Indivirus. Combined, the new viruses add 2,500 additional gene families to the ones previously found in giant viruses.

An evolutionary comparison showed that these viruses were closely related to the Mimivirus family but formed a distinct branch. And compared to the Mimiviruses, they had an even larger collection of genes needed for proteinmanufacture, being able to incorporate 14 of the 20 different amino acids into proteins without any help from the host.

If giant viruses were involved in the origin of life, then the new sequences should shed some light on that. The hypothesis has some consequencesthe viruses should share a core set of genes that are distinct, forming its own domain on the tree of life.

The new study finds very little evidence of that. Instead, as noted above, the new viruses have a lot more protein-manufacturing genes than the Mimiviruses. When the authors analyzed each of these genes individually, they were typically most closely related to a species with a complex cell, rather than another virus. Most of these branches were fairly recent, as well.

In fact, of more than 20 instances of a specific type of gene in the Klosneuvirus, only seven were shared with all the other giant viruses. Only three of those appear to date back to the ancestor of all giant viruses. And only two appear to be distinct enough that they could belong to a distinct branch of the tree of life. The same pattern was apparent in all the other classes of genes involved in making proteins. And, critically, some key components that are used by all branches of life are missing (like the RNAs that are part of the ribosomes, which catalyze protein production.)

In fact, the Klosneuvirus family themselves look like they were stitched together from spare parts. Collectively, the four viruses share 355 genes with species with complex cells. But only 12 of those genes are found in all four of the viruses. Most of them instead seem to have been picked up after the individual virus species split off.

So, the authors propose what they call an "accordion model" of the viruses' evolution. Under some circumstances, the virus goes through periods where it loses genes, slimming down in size somewhat. In other times, the virus picks up new genes, with a preference for certain functions (like preparing amino acids for incorporation into proteins). At the moment, we know too little about the viruses to guess as to what pressures might drive either the expansion or the contraction.

Although the authors don't say as much, however, the fact that they're giant viruses probably makes a big difference in terms of whether that expansion/contraction can happen at all. Many smaller viruses make coats to contain their genetic material that have hard size limitsgeometry dictates that the proteins that form the coat can only come together in specific ways. This size limit, in turn, limits the amount of genetic material that can be squeezed inside. The giant viruses make a correspondingly giant coat, one that may have a lot more flexibility in terms of how much material it can hold.

Science, 2017. DOI: 10.1126/science.aal4657 (About DOIs).

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New giant viruses suggest their genomes expanded like an ... - Ars Technica