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Scientists are exploring why some creatures throw away bits of their DNA during development

To do their lab work, Laura Ross and her team must conduct an itty-bitty surgery. First, they dissect out the reproductive tissues of the black-winged fungus gnat, a diminutive black fly about one-sixteenth to one-eighth of an inch long. Then they home in on particular cells in that tissue: the germ cells, which produce eggs and sperm and so hold the keys to the genome of the next generation.

Ross, an evolutionary biologist at the University of Edinburgh in Scotland, roots around in fungus-gnat parts because theres something odd about the cells in these flies: They dont follow the textbook rules. In sexually reproducing creatures, one full copy of the mothers genetic material generally fuses with one full copy of the fathers to create the complete, doubled-up set of DNA found in cells throughout the body.

But the fungus gnat does something bizarre. Early in the embryos development, most of the cells jettison two specific chromosomes enormous ones, compared with the others so the pair never ends up in the lions share of the gnats body. Only the cells that become germ cells retain the bonus DNA and pass it on to the next generation.

How and why this feature evolved remains largely mysterious, though biologists first spotted it a century ago. And black-winged fungus gnats arent the only genetic screwballs. A surprisingly wide array of creatures, all the way up to some vertebrates, dump significant stretches of DNA during early development, so the stretches dont end up in most of their body cells.

To date, scientists have observed the phenomenon in various insects, in lampreys and hagfish, in hairy one-celled life forms called ciliates, in parasitic roundworms and tiny crustaceans called copepods. Theyve seen it in rat-like marsupials called bandicoots and in songbirds probably all songbirds, according to recent work. And they expect to find many more cases.

A lot of these weird genomic features tend to be fairly rare, but they do evolve repeatedly, Ross says. Its not just one freak event. Presumably, then, there must be some selective advantage to the creatures that go down that evolutionary route. But what is it?

Beyond their fascinating oddness, these quirks may hold broader lessons on how genomes work the way they do, scientists think, and how and why the DNA in germ cells is treated differently from the DNA in the rest of the developing critters body.

Its a fundamental difference between the DNA thats going on to the next generation and the DNA thats in all the other cell types, says Jeramiah Smith, a geneticist at the University of Kentucky who studies the phenomenon in lampreys anddescribed it in the 2020Annual Review of Animal Biosciences.

Starting in the late 1800s, well before scientists nailed down the link between DNA and heredity, biologists peering down microscopes used dyes to study tiny, twig-like bodies inside dividing cells, watching as the twigs grouped together and then separated. German anatomist Wilhelm von Waldeyer-Hartz named these structures chromosomes in 1888, for the ease with which they took up dye.

Around the same time, cell biologists observed chunks of chromosomes being discarded in a parasitic roundworm calledParascaris univalensthat infects horses a much-studied worm because its pair of huge chromosomes were easy to view under a microscope. In later decades, researchers described other worm species that dropped segments from several chromosomes during early rounds of cell division in embryos. But they didnt have the technology to really explore it, says Richard Davis, an emeritus molecular biologist at the University of Colorado School of Medicine in Aurora.

Davis, who dedicated the last decade of his career to studying how this casting-off happens in a handful of roundworms, initially thought that the DNA being eliminated carried no blueprint for any genes. Most biologists (those whove heard of the phenomenon, anyway) have assumed the same thing, he says.

It turned out, though, that this ditched DNA contains genes lots of them. Roundworms from the genus Ascaris, which infect pigs and people, dump about 5 percent of their genes, while those of the genus Parascaris cast off about 10 percent. Only the cells that are destined to form the worms body do the DNA ditching: Just like the black-winged fungus gnat, the full set of genes remain in the cells destined to form eggs and sperm. The worms offspring, and its offsprings offspring, repeat the exact same process.

Davis also noticed something else: Most of the genes that are retained in the germ cellsare active in those cells, implying theyre needed there. And so Davis thinks that tossing the genes away in all the other body cells may be the worms ironclad method of making sure the genes dont become active where they arent meant to.

Guaranteeing that genes are active at certain times but not others, or in some tissues but not others, is a critical function for any living thing. Think of the many different cell types in our bodies: All contain the same DNA sequence, but our heart cells produce different proteins than our skin cells do, so that each can do its specialized job. And even within a particular type of cell, the proteins that are produced vary during a creatures lifespan.

Perhaps what these dropped genes do would be so damaging to adult cells that eliminating them is a better-safe-than-sorry device, Davis says. Its total speculation, though because theres no proof of anything.

But that also presents a puzzler thats yet to be solved. Most living things already have ways to silence specific genes by adding chemical tags. So why do they choose to do this? Davis says.

Smith thinks the same type of extreme gene silencing may be at play in lampreys. His labstumbled upon DNA elimination in these ancient jawless fishwhile working with colleagues on decoding the lamprey genome. Smith had seen research from the 1980s reporting chromosome loss in the closely related hagfish. He decided to see if lampreys were doing the same thing.

Lamprey physiology makes it easy to extract eggs and sperm from the animals Smith likens it to milking a cow or squeezing toothpaste out of a tube. He then fertilized the eggs and watched the embryos develop and found that they were dropping chromosomes 1.5 to 3 days after fertilization.

Lampreys lose 12 entire chromosomes out of their initial set of 96, and perhaps some bits and pieces from the chromosomes that remain. The losses are pre-programmed to occur in almost all the cells of the embryo except for a small handful of cells destined to soon become germ cells. Ultimately, those bits end up in sperm and egg cells, but not in any other lamprey cells.

Using advanced sequencing methods that were just coming online at the time, Smith and his colleagues identified many genes in the eliminated DNA. Intriguingly, about 60 percent to 70 percent of the genes are similar to ones that, in our species, are thought to boost cancer when their activity gets out of control. Whatever their normal function is, those genes might be especially dangerous ones to keep around in body cells. We think lamprey are getting rid of these genes as a means of permanently silencing them, Smith says.

Rosss fungus gnats,Bradysia( Sciara) coprophila, have their own special mystery. They have been bred and maintained for decades, passing from lab to lab. Researchers in the 1920s studying how chromosomes behave in the cell noticed that these flies lose two chromosomes in some cells. (Some insects, its now known, have more than 80 chromosomes to dispose of.) But these chromosomes called germline restricted chromosomes because they are only retained in the germline are almost as large as the rest of the gnats genome.

In fact, theyarebasically an entire genome, as they contain an entire extra set of the genes a gnat has. But fungus gnats are weirder still. When Ross and her team sequenced the chromosomes, she found that the genes they bear arent especially similar to ones of the species they reside in. It looks like the genome of a completely different species, Ross says of an entirely different group of flies.

Rosss best guess is that during a rare mating event between two different species eons ago,the genome of one got integrated into the genome of the otherand somehow got shunted to the germline alone. For her, this still-hypothetical freak event along with other weirdnesses over how flies pass on their genetic material points to a fundamental mystery. The definition of life is being able to copy and paste your genetic material into future generations, she says. Why is this process so variable, and what drives that variation?

That same question drives Alexander Suh, an evolutionary biologist at the University of East Anglia in the UK and Uppsala University in Sweden, who studies a germline-restricted chromosome in the zebra finch, a songbird. Researchers first reported its existence in 1998. As a zebra finch embryo develops, this chromosome somehow magically, says Suh, and I say that with quotes just because I have no explanation yet, gets dropped from all cells except the germ cells.

This bizarre chromosome, too, is chock-full of genes, many of them present in multiple sometimes hundreds of copies. And many are active in the germline.Suh and colleaguesand another groupindependently reported in 2019 that the chromosome dates back to the common ancestor of songbirds, and that all songbirds about half of all birds carry it.

Whatever it is, its been around for 50 million years, Suh says. Its somehow made sure that the host cannot exist without it.

Now Suhs team and others are puzzling out the possible role of this chromosome by looking at the function of the genes it contains. In the zebra finch at least, many of them seem related to development of the female gonad. Others appear to be involved in other aspects of early development.

But its a head scratcher, Suh says, why these genes get passed down in a roundabout way that differs from the standard system of heredity. Smith, Ross and Davis are similarly pondering the reasons for the systems that they study in lampreys, flies and worms.

Perhaps the chromosomes (or bits of chromosomes) are selfish just in it for themselves and have engineered ways to be retained. Or maybe these germline-restricted chromosomes have a benefit for example, by serving as incubators where newly evolved genes are safely housed until it can be determined if theyre beneficial or damaging to the organism.

Alternatively, the processes could be holdovers from earlier evolutionary events. Maybe, says Smith, this silencing technique evolved before or in parallel with some of the silencing methods that vertebrates use today. Is this something that at one period of time defined our ancestors biology?

But whatever the answer or answers turns out to be, its striking, Suh says, how few people, even among biologists, are aware that genes and heredity so often work in peculiar ways.

Maybe, he says, this is something we need to start teaching earlier on: how even more fascinating the genome is than we already thought.

This article originally appeared in Knowable Magazine, an independent journalistic endeavor from Annual Reviews. Sign up for the newsletter.

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The curious case of the shrinking genome - Knowable Magazine

Researchers led by the University of Bath in collaboration with the University of Birmingham observed the evolution of two strains of the soil bacteria Pseudomonas fluorescens (SBW25 and Pf0-1). When the scientists removed a gene that enables the bacteria to swim, both strains of the bacteria quickly evolved the ability to swim again, but using different routes. These findings shed light on how to predict the evolution of bacteria and viruses over time.

The research was published in the journal Nature Communications in a paper titled, A mutational hotspot that determines highly repeatable evolution can be built and broken by silent genetic changes.

Mutational hotspots can determine evolutionary outcomes and make evolution repeatable. Hotspots are products of multiple evolutionary forces including mutation rate heterogeneity, but this variable is often hard to identify, the researchers wrote. In this work, we reveal that a near-deterministic genetic hotspot can be built and broken by a handful of silent mutations.

The researchers compared the DNA sequences of the two strains to understand the differences they observed. They found that in the SBW25 strain, which mutated in a predictable way, there was a region where the DNA strand looped back on itself forming a hairpin-shaped tangle.

Our experiments show that we were able to create or remove mutational hotspots in the genome by altering the sequence to cause or prevent the hairpin tangle, explained Tiffany Taylor, PhD, a research fellow at the Milner Centre for Evolution.This shows that while natural selection is still the most important factor in evolution, there are other factors at play too.

If we knew where the potential mutational hotspots in bacteria or viruses were, it might help us to predict how these microbes could mutate under selective pressure.

This information can help scientists better understand how bacteria and viruses evolve, which can help in developing vaccines against new variants of diseases. It can also make it easier to predict how microbes might develop resistance to antibiotics.

James Horton, PhD, a postdoc at the Milner Centre for Evolution, added: Like many exciting discoveries, this was found by accident. The mutations we were looking at were so-called silent because they dont change the resulting protein sequence, so initially, we didnt think they were particularly important.

However our findings fundamentally challenge our understanding of the role that silent mutations play in adaptation.

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DNA Tangles Found to Create Mutational Hotspots in the Genomes of Bacteria - Genetic Engineering & Biotechnology News

Centre dAnthropobiologie et de Gnomique de Toulouse, Universit Paul Sabatier, Toulouse, France

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Department of the Diversity and Evolution of Genomes, Institute of Molecular and Cellular Biology SB RAS, Novosibirsk, Russia

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W. Szafer Institute of Botany, Polish Academy of Sciences, Krakw, Poland

Tomasz Suchan&Magdalena Moskal-del Hoyo

Genoscope, Institut de biologie Franois-Jacob, Commissariat lEnergie Atomique (CEA), Universit Paris-Saclay, Evry, France

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Gnomique Mtabolique, Genoscope, Institut de biologie Franois Jacob, CEA, CNRS, Universit dEvry, Universit Paris-Saclay, Evry, France

Jean-Marc Aury&Patrick Wincker

Earth System Science Department, University of California, Irvine, Irvine, CA, USA

John Southon

Department of Ecology and Evolutionary Biology, University of California, Santa Cruz, Santa Cruz, CA, USA

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Howard Hughes Medical Institute, University of California, Santa Cruz, Santa Cruz, CA, USA

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Department of Archaeology, Ethnography and Museology, Altai State University, Barnaul, Russia

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Department of Archaeological Heritage Preservation, Institute of Archaeology of the Russian Academy of Sciences, Moscow, Russia

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Zoology Department, College of Science, King Saud University, Riyadh, Saudi Arabia

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Institute for Archaeology, Heritage Conservation Studies and Art History, University of Bamberg, Bamberg, Germany

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Museum stjylland, Randers, Denmark

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Saxo Institute, section of Archaeology, University of Copenhagen, Copenhagen, Denmark

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ArScAn-UMR 7041, Equipe Ethnologie prhistorique, CNRS, MSH-Mondes, Nanterre Cedex, France

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UMR 5199 De la Prhistoire lActuel : Culture, Environnement et Anthropologie (PACEA), CNRS, Universit de Bordeaux, Pessac Cedex, France

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Geneva Natural History Museum, Geneva, Switzerland

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Department of Genetics and Evolution, University of Geneva, Geneva, Switzerland

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OD Earth & History of Life, Royal Belgian Institute of Natural Sciences, Brussels, Belgium

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Institute of Systematics and Evolution of Animals, Polish Academy of Sciences, Krakw, Poland

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Department of Zoology, Institute of Ecology and Earth Sciences, University of Tartu, Tartu, Estonia

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Diamond and Precious Metals Geology Institute, SB RAS, Yakutsk, Russia

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Archaeological Institute of America, Boston, MA, USA

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The origins and spread of domestic horses from the Western Eurasian steppes - Nature.com

Jamaica now has a device that can test for different strains of COVID-19.

Prime Minister Andrew Holness on Friday announcedthat the device a Genome Sequencer is now at the University Hospital of the West Indies.

The long-awaited Genome Sequencer, which will test for different strains for COVID-19, was handed over to the National Influenza Centre at the University Hospital of the West Indies this morning (Friday), Holness said on his social media page.

According to the World Health Organisation (WHOGenomic sequencing has beenimportant for the COVID-19 response.

"New variants are forming all the time, so genomic data has guided countries to make quick and informed public health decisions since the start of the pandemic," a release from WHO has said.

Jamaica recorded 173 new COVID-19 over 24 hours up to Thursday, October 21, according to the Health and Wellness Ministry.

This is while 20 COVID-19 deaths occurred from August 23 to October 19 and were recorded on Thursday, bringing the overall coronavirus death toll in Jamaica to 2,153.

The newly confirmed COVID-19 cases brought the total number on record for the island to 87,970.

And as authorities work to keep cases down Minister of Health and Wellness, DrChristopher Tufton in Septemberannouncedthat the Mu strain of the Coronavirus was in the island.

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Device that can test for different strains of COVID-19 now in Jamaica | Loop Jamaica - Loop News Jamaica

CAMBRIDGE, Mass., Oct. 21, 2021 (GLOBE NEWSWIRE) -- Intellia Therapeutics, Inc. (NASDAQ:NTLA), a leading clinical-stage genome editing company focused on developing curative therapeutics using CRISPR/Cas9 technology both in vivo and ex vivo, announced today that the U.S. Food and Drug Administration (FDA) has granted orphan drug designation to NTLA-2001 for the treatment of transthyretin (ATTR) amyloidosis. This investigational therapy is the first CRISPR therapy to be administered systemically to edit a disease-causing gene inside the human body. NTLA-2001 has the potential to be the first single-dose treatment for ATTR amyloidosis as it may be able to halt and reverse the devastating complications of this disease. ATTR amyloidosis is a rare condition that can impact a number of organs and tissues within the body through the accumulation of misfolded transthyretin (TTR) protein deposits.

Orphan drug designation underscores the FDAs recognition of NTLA-2001s potential promise as a single-dose, novel therapy for the treatment of ATTR amyloidosis, said Intellia President and Chief Executive Officer John Leonard, M.D. At Intellia, we are committed to advancing our modular genome editing platform to develop potentially curative treatment options for life-threatening diseases, and we look forward to working with the ATTR amyloidosis community and the FDA to bring a much-needed treatment option to patients.

NTLA-2001 is currently being studied in a Phase 1 trial in adults with hereditary ATTR amyloidosis with polyneuropathy (ATTRv-PN). In June 2021, Intellia and its collaborator Regeneron announced positive interim clinical results from the first two cohorts of this study. These results, which were published in the New England Journal of Medicine, represented the first-ever clinical data supporting the safety and efficacy of in vivo CRISPR genome editing in humans.

The FDA's Orphan Drug Designation program provides orphan status to drugs defined as those intended for the treatment, diagnosis or prevention of rare diseases that affect fewer than 200,000 people in the United States. Orphan drug designation qualifies the sponsor of the drug for certain development incentives, including tax credits for qualified clinical testing, prescription drug user fee exemptions and seven-year marketing exclusivity upon FDA approval. The decision by the FDA follows a March 2021 decision by the European Commission (EC) to also grant NTLA-2001 orphan drug designation for the treatment of ATTR amyloidosis.

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About Transthyretin (ATTR) Amyloidosis Transthyretin amyloidosis, or ATTR amyloidosis, is a rare, progressive and fatal disease. Hereditary ATTR (ATTRv) amyloidosis occurs when a person is born with mutations in the TTR gene, which causes the liver to produce structurally abnormal transthyretin (TTR) protein with a propensity to misfold. These damaged proteins build up as amyloid deposits in the body, causing serious complications in multiple tissues, including the heart, nerves and digestive system. ATTRv amyloidosis predominantly manifests as polyneuropathy (ATTRv-PN), which can lead to nerve damage, or cardiomyopathy (ATTRv-CM), which can lead to heart failure. Some individuals without any genetic mutation produce non-mutated, or wild-type TTR proteins that become unstable over time, misfolding and aggregating in disease-causing amyloid deposits. This condition, called wild-type ATTR (ATTRwt) amyloidosis, primarily affects the heart.

About NTLA-2001Based on Nobel Prize-winning CRISPR/Cas9 technology, NTLA-2001 could potentially be the first curative treatment for ATTR amyloidosis. NTLA-2001 is the first investigational CRISPR therapy candidate to be administered systemically, or intravenously, to edit genes inside the human body. Intellias proprietary non-viral platform deploys lipid nanoparticles to deliver to the liver a two-part genome editing system: guide RNA specific to the disease-causing gene and messenger RNA that encodes the Cas9 enzyme, which carries out the precision editing. Robust preclinical data, showing deep and long-lasting transthyretin (TTR) reduction following in vivo inactivation of the target gene, supports NTLA-2001s potential as a single-administration therapeutic. Interim Phase 1 clinical data released in June 2021 confirm substantial, dose-dependent reduction of TTR protein following a single dose of NTLA-2001. Intellia leads development and commercialization of NTLA-2001 as part of a multi-target discovery, development and commercialization collaboration with Regeneron.

About Intellia TherapeuticsIntellia Therapeutics, a leading clinical-stage genome editing company, is developing novel, potentially curative therapeutics using CRISPR/Cas9 technology. To fully realize the transformative potential of CRISPR/Cas9, Intellia is pursuing two primary approaches. The companys in vivo programs use intravenously administered CRISPR as the therapy, in which proprietary delivery technology enables highly precise editing of disease-causing genes directly within specific target tissues. Intellias ex vivo programs use CRISPR to create the therapy by using engineered human cells to treat cancer and autoimmune diseases. Intellias deep scientific, technical and clinical development experience, along with its robust intellectual property portfolio, have enabled the company to take a leadership role in harnessing the full potential of CRISPR/Cas9 to create new classes of genetic medicine. Learn more at intelliatx.com. Follow us on Twitter @intelliatweets.

Forward-Looking StatementsThis press release contains forward-looking statements of Intellia Therapeutics, Inc. (Intellia or the Company) within the meaning of the Private Securities Litigation Reform Act of 1995. These forward-looking statements include, but are not limited to, express or implied statements regarding Intellias beliefs and expectations regarding its: being able to complete clinical studies for NTLA-2001 for the treatment of transthyretin (ATTR) amyloidosis pursuant to its clinical trial applications (CTA), including submitting additional regulatory applications in other countries; ability to demonstrate effectiveness of NTLA-2001 in treating or reversing ATTR amyloidosis in patients; advancement and expansion of its CRISPR/Cas9 technology to develop human therapeutic products, as well as its ability to maintain and expand its related intellectual property portfolio; expectations of the potential impact of the coronavirus disease 2019 pandemic on strategy, future operations and timing of its clinical trials or IND submissions; ability to optimize the impact of its collaborations on its development programs, including but not limited to its collaborations with Regeneron, including its co-development programs for ATTR amyloidosis; and statements regarding the timing of regulatory filings regarding its development programs.

Any forward-looking statements in this press release are based on managements current expectations and beliefs of future events and are subject to a number of risks and uncertainties that could cause actual results to differ materially and adversely from those set forth in or implied by such forward-looking statements. These risks and uncertainties include, but are not limited to: risks related to Intellias ability to protect and maintain its intellectual property position; risks related to Intellias relationship with third parties, including its licensors and licensees; risks related to the ability of its licensors to protect and maintain their intellectual property position; uncertainties related to the authorization, initiation and conduct of studies and other development requirements for its product candidates; the risk that any one or more of Intellias product candidates will not be successfully developed and commercialized; the risk that the results of preclinical studies or clinical studies will not be predictive of future results in connection with future studies; and the risk that Intellias collaborations with Regeneron or its other collaborations will not continue or will not be successful. For a discussion of these and other risks and uncertainties, and other important factors, any of which could cause Intellias actual results to differ from those contained in the forward-looking statements, see the section entitled Risk Factors in Intellias most recent annual report on Form 10-K as well as discussions of potential risks, uncertainties, and other important factors in Intellias other filings with the Securities and Exchange Commission (SEC). All information in this press release is as of the date of the release, and Intellia undertakes no duty to update this information unless required by law.

Intellia Contacts:

Investors:Ian KarpSenior Vice President, Investor Relations and Corporate Communications+1-857-449-4175ian.karp@intelliatx.com

Lina LiDirector, Investor Relations+1-857-706-1612lina.li@intelliatx.com

Media:Lisa QuTen Bridge Communications+1-678-662-9166media@intelliatx.com lqu@tenbridgecommunications.com

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Intellia Therapeutics Receives U.S. FDA Orphan Drug Designation for NTLA-2001, an Investigational CRISPR Therapy for the Treatment of Transthyretin...