Category Archives: Genome

WORCESTER A group that includes local researchers has sequenced the genome of a hookworm that infects both humans and animals, an advance that could add to efforts to develop vaccines and treatments to defeat the parasite.

The scientists reported Monday in the journal Nature Genetics that they identified nearly 31,000 active genes in the tiny blood-sucking worm known as Ancylostoma ceylanicum. They also identified a family of genes that might be important to a worm's infection process.

Raffi V. Aroian, a professor in molecular medicine at the University of Massachusetts Medical School, said he and lead author Erich M. Schwarz, a senior research associate at Cornell University, conceived the project to better understand a class of parasites that causes anemia and suffering.

"Know thy enemy, right?" Mr. Aroian said. "In other words, we learned a lot by sequencing the human genome. Modern medicine wouldn't be where it's at at all without the genome. In our case, it's knowing the genome of the parasite so we can determine what its potential weaknesses are."

A 2014 study estimated nearly 439 million people worldwide were infected with hookworms, small creatures that can live for years in the bodies of hosts. Infection is mostly found in tropical developing countries with poor sanitation.

Larvae, or immature worms, live in soil contaminated by feces from infected people. The larvae can burrow into the bare feet of humans, then travel to the intestines where they feed on blood, mature, mate and produce eggs.

Infected humans can develop anemia. Hookworm infection also can stunt the growth and development of children.

Although a drug exists to treat infection, hookworm infection is so common in parts of the world that it is thought to have a negative effect on economies.

The new genome sequence is not the first time a hookworm's genetic code has been unraveled. A large international group of researchers reported last year they had sequenced the genome of Necator americanus, the type of hookworm most commonly responsible for human infection.

But the new research concerns a hookworm known to afflict a number of mammals, not just people, said Mr. Schwarz.

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UMass Medical researchers unravel hookworm genome, could deal blow to parasite

WORCESTER A group that includes local researchers has sequenced the genome of a type of worm known for infecting millions worldwide, a step that could aid scientists who are working on vaccines and treatments.

Raffi V. Aroian, a professor in molecular medicine at the University of Massachusetts Medical School, and UMass Researcher Assistant Professor Yan Hu were part of a team that found the blood-sucking hookworm known as A. ceylanicum has about 30,000 genes, according to an article published online Monday by the journal Nature Genetics. The team identified dozens of genes that might be targets for drug and vaccine studies.

Erich M. Schwarz of Cornell University, the study's lead author, and Mr. Aroian conceived the project to better understand a class of parasites that causes anemia and suffering, Mr. Aroian said.

"Know thy enemy, right?" Mr. Aroian said. "In other words, we learned a lot by sequencing the human genome. Modern medicine wouldn't be where it's at at all without the genome. In our case, it's knowing the genome of the parasite so we can determine what its potential weaknesses are."

Hookworm infection is mostly found in tropical and developing countries with poor hygiene and sanitation. The immature worms, or larvae, live in soil contaminated by feces from infected people.

The worms can burrow into the bare feet of humans, then travel to the intestines where they feed on blood, mature, mate and produce eggs.

The World Health Organization estimated in 2009 that 2 billion people worldwide were infected with soil-transmitted worms, including hookworms.

Contact Lisa Eckelbecker at lisa.eckelbecker@telegram.com. Follow her on Twitter @LisaEckelbecker.

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UMMS researchers sequence hookworm genome

2 hours ago A female Hessian fly dangles from a cardboard box. Fly larvae can decimate entire wheat fields by causing growth-stunting galls on seedlings. Credit: Purdue University / Tom Campbell

A team of researchers from 26 institutions around the world has sequenced the Hessian fly genome, shedding light on how the insect creates growth-stunting galls in wheat.

Hessian fly larvae can destroy entire wheat fields by injecting seedlings with potent saliva that "hijacks" the plants' biochemistry, irreversibly halting development and forcing the seedlings to produce a leaky tissue that contains nutrients for the larvae.

But how the insect is able to slip past plant defenses to create these galls - that is, the plant's stunted growth - has not been well understood.

The genome reveals that the Hessian fly has an extensive reservoir of rapidly evolving genes that code for effector proteins, molecules that control gene expression and cell signaling. The structures of these proteins are remarkably similar to proteins in plants, said study co-author Jeffrey Stuart, which suggests that they mimic normal proteins in the plant cell and use this disguise to manipulate wheat seedling biochemistry.

"The Hessian fly is basically a plant pathogen in the shape of an insect," said Stuart, professor of insect molecular genetics at Purdue. "If we have a deeper understanding of how the insect is attacking the plant and how it avoids detection, we may be able to develop new ways of making resistant wheat more durable and better advise growers on which varieties to plant."

Likely native to the Middle East, the Hessian fly is a pest of global importance. Wheat genetic resistance to the insect is particularly desirable in regions where cultural control methods, such as late planting, are not an option.

"In a few days, a single larva can transform a healthy wheat seedling into one that won't grow anymore," Stuart said.

But wheat is not without its own defenses. Stuart said at least 35 genes in wheat can detect and identify an effector protein injected by the Hessian fly and trigger a counterattack: The plant can thicken its cell wall, preventing fly larvae from extracting nutrients, and produce toxic substances to dispatch the pest. In the southern U.S., some growers use wheat with specific resistance genes to manage Hessian fly.

But the resistance typically fades after 5-10 years as Hessian fly populations that are unable to survive on resistant wheat die off and are replaced by populations with effector proteins that the plant cannot recognize.

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Genome reveals how Hessian fly causes galls in wheat

James Watson, Personal Genome Pioneer, Interviewed by Robert Krulwich and Carl Zimmer - Part 2 of 12
In 2010, we brought together, on one stage, nearly everyone in the world whose full genome had been sequenced. We knew that, with the pace of genome sequenci...

By: PersonalGenomesOrg

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James Watson, Personal Genome Pioneer, Interviewed by Robert Krulwich and Carl Zimmer - Part 2 of 12 - Video

Personal Genome Pioneers and thought leaders interviewed by Krulwich and Zimmer - Part 9 of 12
In 2010, we brought together, on one stage, nearly everyone in the world whose full genome had been sequenced. We knew that, with the pace of genome sequenci...

By: PersonalGenomesOrg

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Personal Genome Pioneers and thought leaders interviewed by Krulwich and Zimmer - Part 9 of 12 - Video

Personal Genome Pioneers interviewed by Robert Krulwich and Carl Zimmer - Part 4 of 12
In 2010, we brought together, on one stage, nearly everyone in the world whose full genome had been sequenced. We knew that, with the pace of genome sequenci...

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Personal Genome Pioneers interviewed by Robert Krulwich and Carl Zimmer - Part 4 of 12 - Video

Whole genome profiling - superior plant genome assembly
In this video, KeyGene shows the added value of combining the whole genome profiling technology and long read sequences produced by the PacBio.

By: KeyGeneInfo

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Whole genome profiling - superior plant genome assembly - Video

Once HIV-1 has hijacked a host cell to make copies of its own RNA genome and viral proteins, it must assemble these components into new virus particles. The orchestration of this intricate assembly process falls to a viral protein known as Gag. For one thing, Gag must be able to discern viral RNA from the host cell's and squirrel it away inside new viral particles -- no easy task considering only two to three percent of the RNA found in the cytoplasm is from HIV-1. Exactly how Gag selectively packages viral RNA has been widely speculated but never directly observed.

Now a team of researchers from Paul Bieniasz's Laboratory of Retrovirology at The Rockefeller University and the Aaron Diamond AIDS Research Center have employed a recently developed technique to capture -- in a sort of molecular freeze-frame -- just how Gag accomplishes this feat. In research published recently in Cell, they reveal that Gag undergoes dramatic and transient changes in binding preferences that allow it to precisely select viral RNA for packaging into new viruses.

"One of the functions of Gag is to choose the viral RNA from all the RNA present in the cell to package into a viral particle, which will then go on to infect a new cell," say Bieniasz. Gag, the major structural protein of HIV-1, floats about as individual molecules in the cytoplasm, but to assemble new viruses, thousands of Gag coalesce at the host cell's plasma membrane, forming an immature viral particle containing two strands of viral RNA.

Previous studies suggested that Gag targeted viral RNA by binding to a sequence known as psi, but many suspected that this interaction alone could not account for Gag's ability to discriminate between viral and host cell RNA.

To observe just how Gag recruits viral RNA, the researchers turned to a technique known as crosslinking-immunoprecipitation (CLIP) sequencing, which uses ultraviolet light to fuse RNA and protein and preserve interactions for further analysis. "CLIP essentially freezes the interaction in space and time, and tells you in a very localized, specific way the RNA sequences your protein was bound to," says first author Sebla B. Kutluay, a postdoctoral fellow in the lab.

Gag does indeed bind to psi on viral RNA, the researchers found, the first time this interaction has been demonstrated in a biologically relevant setting. But as they suspected, there was more to the story. When Gag moves to the plasma membrane, it appears to completely change its behavior and bind to many different sites throughout the HIV-1 genome.

By analyzing the RNA sequences bound by Gag, the researchers discovered that the protein seems to change its taste for nucleotides depending on location. Gag in the cytoplasm prefers RNA sequences rich in guanine, but at the plasma membrane, Gag is temporarily drawn to sequences rich in adenine. Strikingly, the genome of HIV-1 is particularly adenine-rich -- an unusual property of the HIV-1 genome that has heretofore puzzled scientists.

Such changes in RNA binding behavior would have been impossible to observe even a few years ago, before the availability of CLIP. "Gag binding to adenine-rich RNAs was never seen before by any approach and could not have been seen by any other approach," says Bieniasz, noting that CLIP was developed by colleagues in Robert B. Darnell's laboratory and refined in Thomas Tuschl's laboratory at Rockefeller.

The sudden switch in RNA binding appears to be multimerization-dependent -- that is, induced by the crowding of Gag at the plasma membrane, which may block certain proteins surfaces and alter binding behavior.

"It's the first example of an RNA binding protein that shows such dramatic changes in specificity depending on where it is in the cell," says Bieniasz. "It really changes the way we understand how HIV packages its genome."

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Transient details of HIV genome packaging captured

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Newswise Once HIV-1 has hijacked a host cell to make copies of its own RNA genome and viral proteins, it must assemble these components into new virus particles. The orchestration of this intricate assembly process falls to a viral protein known as Gag. For one thing, Gag must be able to discern viral RNA from the host cells and squirrel it away inside new viral particles no easy task considering only two to three percent of the RNA found in the cytoplasm is from HIV-1. Exactly how Gag selectively packages viral RNA has been widely speculated but never directly observed.

Now a team of researchers from Paul Bieniaszs Laboratory of Retrovirology at The Rockefeller University and the Aaron Diamond AIDS Research Center have employed a recently developed technique to capture in a sort of molecular freeze-frame just how Gag accomplishes this feat. In research published recently in Cell, they reveal that Gag undergoes dramatic and transient changes in binding preferences that allow it to precisely select viral RNA for packaging into new viruses.

One of the functions of Gag is to choose the viral RNA from all the RNA present in the cell to package into a viral particle, which will then go on to infect a new cell, say Bieniasz. Gag, the major structural protein of HIV-1, floats about as individual molecules in the cytoplasm, but to assemble new viruses, thousands of Gag coalesce at the host cells plasma membrane, forming an immature viral particle containing two strands of viral RNA.

Previous studies suggested that Gag targeted viral RNA by binding to a sequence known as psi, but many suspected that this interaction alone could not account for Gags ability to discriminate between viral and host cell RNA.

To observe just how Gag recruits viral RNA, the researchers turned to a technique known as crosslinking-immunoprecipitation (CLIP) sequencing, which uses ultraviolet light to fuse RNA and protein and preserve interactions for further analysis. CLIP essentially freezes the interaction in space and time, and tells you in a very localized, specific way the RNA sequences your protein was bound to, says first author Sebla B. Kutluay, a postdoctoral fellow in the lab.

Gag does indeed bind to psi on viral RNA, the researchers found, the first time this interaction has been demonstrated in a biologically relevant setting. But as they suspected, there was more to the story. When Gag moves to the plasma membrane, it appears to completely change its behavior and bind to many different sites throughout the HIV-1 genome.

By analyzing the RNA sequences bound by Gag, the researchers discovered that the protein seems to change its taste for nucleotides depending on location. Gag in the cytoplasm prefers RNA sequences rich in guanine, but at the plasma membrane, Gag is temporarily drawn to sequences rich in adenine. Strikingly, the genome of HIV-1 is particularly adenine-rich an unusual property of the HIV-1 genome that has heretofore puzzled scientists.

Such changes in RNA binding behavior would have been impossible to observe even a few years ago, before the availability of CLIP. Gag binding to adenine-rich RNAs was never seen before by any approach and could not have been seen by any other approach, says Bieniasz, noting that CLIP was developed by colleagues in Robert B. Darnells laboratory and refined in Thomas Tuschls laboratory at Rockefeller.

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Research Captures Transient Details of HIV Genome Packaging

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Osu! - Tsunamaru - Daidai Genome [Insane] w/ DT - 211pp - Video