Hexbyte Glen Cove New cause found for intensification of oyster disease thumbnail

Hexbyte Glen Cove New cause found for intensification of oyster disease

Hexbyte Glen Cove

Panel A shows the original form of the Dermo parasite Perkinsus marinus, with black arrows indicating typical Dermo cells and the white arrow a dividing form, all infecting connective tissues deep inside an oyster. Panel B shows the new form of the parasite, much smaller, with the arrow indicating a mass of dozens of Dermo cells inside a single oyster blood cell, and primarily infecting the lining of the stomach and gut. Credit: R. Carnegie/VIMS.

A new paper in Scientific Reports led by researchers at William & Mary’s Virginia Institute of Marine Science challenges increased salinity and seawater temperatures as the established explanation for a decades-long increase in the prevalence and deadliness of a major oyster disease in the coastal waters of the mid-Atlantic.

Dr. Ryan Carnegie, the paper’s lead author, says “We present an entirely new lens through which we can view our last 35 years of history in the Chesapeake Bay region. We now know the great intensification of Dermo disease in the 1980s wasn’t simply due to drought. It was more fundamentally due to the emergence of a new and highly virulent form of Perkinsus marinus, the parasite that causes Dermo.”

In an unusual twist, the team’s evidence suggests that transformation of this native parasite was in response to evolutionary pressures brought by the impacts of another, non-native oyster parasite known as MSX, first seen in Bay waters in 1959. Dermo’s mid-80s rise in virulence, along with decades of overharvesting, habitat destruction, and the earlier devastation of MSX, brought the Bay’s traditional oyster fishery to a historic low.

Carnegie says his team’s findings can help better manage the Bay’s modern oyster industry, which is now on the upswing due to disease-resistant aquaculture strains, reef restoration, and limits on the wild harvest. “The lesson,” he says, “is that pathogens like P. marinus are highly dynamic, and our disease surveillance must be attentive to any changes that may occur. This includes the emergence of more virulent strains, or variants that may have different forms or life histories than we expect. Management should be continually tuned to any changes in disease dynamics.”

The team’s findings also give scientists and fishery managers a better understanding of the “rock-bottom” era for Bay oysters between the late 1980s and early 2000s. “The oysters reached this level of devastation not because they were unable to deal with Dermo after decades, if not centuries or millennia, of exposure,” says Carnegie. “They hit rock bottom because they were challenged with a brand-new form of the parasite, and needed time to adapt. And now they are adapting, which is key to the oyster’s recent recovery in the region.”

Along with Carnegie, the paper’s other authors are the late Susan Ford of Haskin Shellfish Research Laboratory at Rutgers University; Peter Kingsley-Smith of the South Carolina Department of Natural Resources; and Rita Crockett, Lydia Bienlien, Lúcia Safi, Laura Whitefleet-Smith, and Eugene Burreson of VIMS. Funding for the study comes from the VIMS Foundation A. Marshall Acuff, Sr., Memorial Endowment for Oyster Disease Research.

The sharp transition from the original form of Dermo (light blue) to contemporary (dark blue) in Chesapeake Bay (A), South Carolina (B), and New Jersey (C). Weighted prevalence in the Virginia panel is a conventional measure of Dermo disease in oyster populations, and shows that the change in Dermo’s form in Virginia coincided with the increase in Dermo prevalence within Bay oysters. Credit: © R. Carnegie/VIMS.

Evidence for a more virulent Dermo parasite

Dermo disease results when the eastern oyster Crassostrea virginica is infected by the protozoan parasite Perkinsus marinus. Infected oysters grow more slowly, exhibit poorer body condition, and reproduce less successfully than their healthy counterparts. Severe infections lead to oyster death and release of into the surrounding water, potentially infecting other nearby oysters as they filter water for food. The disease does not affect people who eat the shellfish.

Native to the Gulf Coast, Dermo was first recorded in the Chesapeake Bay in 1949, though it had likely been there far longer. Prior to the 1980s, it typically occurred as a chronic disease that killed about 30% of oysters annually, mostly older animals that had been exposed to the parasite for several years. But, says Carnegie, “around 1986, Dermo suddenly became an acute and profoundly destructive disease capable of killing more than 70% of host oysters within months of infection.” The increased virulence of the Perkinsus parasite persists today.

Because the parasite’s infectiousness is known to increase with higher salinity, scientists initially attributed the mid-1980s spike in Dermo’s virulence to a multi-year drought that had struck the mid-Atlantic around that time, raising coastal salinities as freshwater input from rivers decreased. Increasing seawater temperatures also promote increased Dermo disease, and ocean warming has been blamed for the northward increase in Dermo’s range since the 1980s. As time passed, however, Carnegie and other researchers began to realize that salinity and temperature alone did not fully explain the lasting increase in Dermo infections and associated oyster mortality along the East Coast.

“We began to ask why more protracted and intense droughts in earlier years, before the 1980s, hadn’t produced a similar intensification of disease,” says Carnegie, “and why subsequent wet periods didn’t return the parasite to the low levels of infection characteristic of earlier years.”

Motivated by these questions, Carnegie and colleagues compared samples from modern Bay oysters with samples taken in 1960 and stored at VIMS, using paper-thin tissue slices glued onto slides for viewing under a microscope. Finding striking and unexpected differences, they then took a comprehensive look at more than 8,000 tissue samples collected from oysters in Chesapeake Bay, South Carolina, and New Jersey between 1960 and 2018.

“Our analysis,” says Carnegie, “clearly showed that a new parasite variant emerged between 1983 and 1990, concurrent with the historical mid-80s outbreaks of Dermo.” Changes included a shift in the infection site—from deeper connective tissues to the lining of the digestive tract—changes in reproductive strategy, and a sharp decrease in cell size. In Chesapeake Bay, they found the most pronounced change between oysters sampled in 1985 and 1986, when the modern variant increased in frequency from 22% to 99% of observations.

Dr. Ryan Carnegie (L) of the Virginia Institute of Marine Science and postdoctoral research associate Lúcia Safi collect oysters from the waters of the Chesapeake Bay as part of their long-term study of Dermo disease. Credit: © P. Richardson/VIMS.

“The picture that emerges,” says Carnegie, “is the rise of a virulent new form of the Dermo parasite Perkinsus along the mid-Atlantic coast in the mid-80s, which dispersed from there and supplanted a form that previously had been widely distributed in Atlantic estuaries. While changes in pathogen virulence have been documented in other systems, the scope of changes we’ve seen, and their rapid spread across a wide area, is unusual.”

“Our work underscores the importance of long-term environmental monitoring,” he adds. “Without that, and the maintenance of associated natural history collections, this new perspective wouldn’t have been possible.”

Evolutionary pressures

The type of changes observed in the Dermo parasite suggest they represent a novel but predictable response to the devastating impacts of MSX, the disease caused by the non-native parasite Haplosporidium nelsoni, which was first reported in Bay waters in 1959. MSX killed more than 90% of Virginia’s farmed oysters by 1961, and slashed the harvest of planted oysters from 3,347,170 bushels in 1959 to 361,792 bushels by 1983, an estimated loss of 1.8 billion animals. This decrease was likely compounded by simultaneous losses from wild populations.

A parasite that quickly kills its host effectively destroys its own home. Over evolutionary time scales, natural selection thus often leads to an equilibrium between a native parasite and its host, marked by the type of minor, long-term Perkinsus infections and low rates of Dermo mortality historically observed in Chesapeake Bay oysters.

But when a new parasite arrives on the scene, that evolutionary balance may shift. Carnegie and his team speculate that the devastating arrival of the non-native, MSX parasite in Bay waters drastically disrupted the long-established equilibrium between Dermo and Crassostrea, directly leading to the new, more virulent form of the disease.

“A huge reduction in oyster abundance—like that caused by the arrival of MSX—would severely impact a parasite such as P. marinus that depends entirely on a single host,” says Carnegie. As evidence, he notes that Perkinsus declined sharply in abundance beginning in 1959; recent theoretical modeling underscores the possibility that an increase in parasite virulence could be a consequence of such reduction in host resources.

“The changes we saw in the Dermo parasite are likely adaptive with regard to the reduced oyster abundance and longevity it faced after rapid establishment of Haplosporidium nelsoni and MSX in 1959,” says Carnegie. “Our findings, we hypothesize, illustrate a novel ecosystem response to a marine parasite invasion: an increase in virulence in a native parasite.” An intriguing possibility is that the changes the researchers observed may represent a shortening of the Perkinsus life cycle, as it adapted to oysters with shorter life spans due to mortality from MSX.

More information:
Ryan B. Carnegie et al, A rapid phenotype change in the pathogen Perkinsus marinus was associated with a historically significant marine disease emergence in the eastern oyster, Scientific Reports (2021). DOI: 10.1038/s41598-021-92379-6

New cause found for intensification of oyster disease (2021, June 18)
retrieved 21 June 2021
from https://phys.org/news/2021-06-intensification-oyster-disease.html

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Hexbyte Glen Cove Found in space: Complex carbon-based molecules thumbnail

Hexbyte Glen Cove Found in space: Complex carbon-based molecules

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The Taurus Molecular Cloud, which contains the cold starless core TMC-1, is a dark streak on the sky near the Pleiades cluster as seen from Charlottesville, VA. Credit: Brett A. McGuire, Copyright 2018

Much of the carbon in space is believed to exist in the form of large molecules called polycyclic aromatic hydrocarbons (PAHs). Since the 1980s, circumstantial evidence has indicated that these molecules are abundant in space, but they have not been directly observed.

Now, a team of researchers led by MIT Assistant Professor Brett McGuire has identified two distinctive PAHs in a patch of space called the Taurus Molecular Cloud (TMC-1). PAHs were believed to form efficiently only at high temperatures—on Earth, they occur as byproducts of burning fossil fuels, and they’re also found in char marks on grilled food. But the interstellar cloud where the research team observed them has not yet started forming stars, and the temperature is about 10 degrees above absolute zero.

This discovery suggests that these molecules can form at much lower temperatures than expected, and it may lead scientists to rethink their assumptions about the role of PAH chemistry in the formation of stars and planets, the researchers say.

“What makes the detection so important is that not only have we confirmed a hypothesis that has been 30 years in the making, but now we can look at all of the other molecules in this one source and ask how they are reacting to form the PAHs we’re seeing, how the PAHs we’re seeing may react with other things to possibly form larger molecules, and what implications that may have for our understanding of the role of very large carbon molecules in forming planets and stars,” says McGuire, who is a senior author of the new study.

Michael McCarthy, associate director of the Harvard-Smithsonian Center for Astrophysics, is another senior author of the study, which appears today in Science. The research team also includes scientists from several other institutions, including the University of Virginia, the National Radio Astronomy Observatory, and NASA’s Goddard Space Flight Center.

Distinctive signals

Starting in the 1980s, astronomers have used telescopes to detect infrared signals that suggested the presence of aromatic molecules, which are molecules that typically include one or more carbon rings. About 10 to 25 percent of the carbon in space is believed to be found in PAHs, which contain at least two , but the infrared signals weren’t distinct enough to identify specific molecules.

“That means that we can’t dig into the detailed chemical mechanisms for how these are formed, how they react with one another or other molecules, how they’re destroyed, and the whole cycle of carbon throughout the process of forming stars and planets and eventually life,” McGuire says.

Although radio astronomy has been a workhorse of molecular discovery in space since the 1960s, radio telescopes powerful enough to detect these large molecules have only been around for a little over a decade. These telescopes can pick up molecules’ rotational spectra, which are distinctive patterns of light that molecules give off as they tumble through space. Researchers can then try to match patterns observed in space with patterns that they have seen from those same molecules in laboratories on Earth.

The 100-m Green Bank Telescope located in Green Bank, WV. Credit: Brett A. McGuire, Copyright 2018

“Once you have that pattern match, you know there is no other molecule in existence that could be giving off that exact spectrum. And, the intensity of the lines and the relative strength of the different pieces of the pattern tells you something about how much of the molecule there is, and how warm or cold the molecule is,” McGuire says.

McGuire and his colleagues have been studying TMC-1 for several years because previous observations have revealed it to be rich in complex carbon molecules. A few years ago, one member of the research team observed hints that the cloud contain benzonitrile—a six-carbon ring attached to a nitrile (carbon-nitrogen) group.

The researchers then used the Green Bank Telescope, the world’s largest steerable radio telescope, to confirm the presence of benzonitrile. In their data, they also found signatures of two other molecules—the PAHs reported in this study. Those molecules, called 1-cyanonaphthalene and 2-cyanonaphthalene, consist of two benzene rings fused together, with a nitrile group attached to one ring.

“Detecting these molecules is a major leap forward in astrochemistry. We are beginning to connect the dots between small molecules—like benzonitrile—that have been known to exist in space, to the monolithic PAHs that are so important in astrophysics,” says Kelvin Lee, an MIT postdoc who is one of the authors of the study.

Finding these molecules in the cold, starless TMC-1 suggests that PAHs are not just the byproducts of dying stars, but may be assembled from smaller molecules.

“In the place where we found them, there is no star, so either they’re being built up in place or they are the leftovers of a dead star,” McGuire says. “We think that it’s probably a combination of the two—the evidence suggests that it is neither one pathway nor the other exclusively. That’s new and interesting because there really hadn’t been any observational evidence for this bottom-up pathway before.”

In a series of nine papers, scientists from the GOTHAM–Green Bank Telescope Observations of TMC-1: Hunting Aromatic Molecules–project described the detection of more than a dozen polycyclic aromatic hydrocarbons in the Taurus Molecular Cloud, or TMC-1. These complex molecules, never before detected in the interstellar medium, are allowing scientists to better understand the formation of stars, planets, and other bodies in space. In this artist’s conception, some of the detected molecules include, from left to right: 1-cyanonaphthalene, 1-cyano-cyclopentadiene, HC11N, 2-cyanonaphthalene, vinylcyanoacetylene, 2-cyano-cyclopentadiene, benzonitrile, trans-(E)-cyanovinylacetylene, HC4NC, and propargylcyanide, among others. Credit: M. Weiss / Center for Astrophysics | Harvard & Smithsonian

Carbon chemistry

Carbon plays a critical role in the formation of planets, so the suggestion that PAHs might be present even in starless, cold regions of space, may prompt scientists to rethink their theories of what chemicals are available during planet formation, McGuire says. As PAHs react with other molecules, they may start to form interstellar dust grains, which are the seeds of asteroids and planets.

“We need to entirely rethink our models of how the chemistry is evolving, starting from these starless cores, to include the fact that they are forming these large aromatic molecules,” he says.

McGuire and his colleagues now plan to further investigate how these PAHs formed, and what kinds of reactions they may undergo in . They also plan to continue scanning TMC-1 with the powerful Green Bank Telescope. Once they have those observations from the , the researchers can try to match up the signatures they find with data that they generate on Earth by putting two molecules into a reactor and blasting them with kilovolts of electricity, breaking them into bits and letting them recombine. This could result in hundreds of different molecules, many of which have never been seen on Earth.

“We need to continue to see what are present in this interstellar source, because the more we know about the inventory, the more we can start trying to connect the pieces of this reaction web,” McGuire says.

More information:
B.A. McGuire el al., “Detection of two interstellar polycyclic aromatic hydrocarbons via spectral matched filtering,” Science (2021). science.sciencemag.org/cgi/doi … 1126/science.abb7535

Ci Xue et al. Detection of Interstellar HC4NC and an Investigation of Isocyanopolyyne Chemistry under TMC-1 Conditions, The Astrophysical Journal (2020). iopscience.iop.org/article/10. … 847/2041-8213/aba631

Brett A. McGuire et al. Early Science from GOTHAM: Project Overview, Methods, and the Detection of Interstellar Propargyl Cyanide (HCCCH2CN) in TMC-1, The Astrophysical Journal (2020). iopscience.iop.org/article/10. … 847/2041-8213/aba632

Andrew M. Burkhardt et al. Ubiquitous aromatic carbon chemistry at the earliest stages of star formation, Nature Astronomy (2021). DOI: 10.1038/s41550-020-01253-4

Michael C. McCarthy et al. Interstellar detection of the highly polar five-membered ring cyanocyclopentadiene, Nature Astronomy (2020). DOI: 10.1038/s41550-020-01213-y

Found in space: Complex carbon-based molecules (2021, March 18)
retrieved 19 March 2021
from https://phys.org/news/2021-03-space-complex-carbon-based-molecules.html

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Hexbyte Glen Cove New activity found for CHD7, a protein factor vital in embryonic development thumbnail

Hexbyte Glen Cove New activity found for CHD7, a protein factor vital in embryonic development

Hexbyte Glen Cove

A colony of embryonic stem cells, from the H9 cell line (NIH code: WA09). Viewed at 10X with Carl Zeiss Axiovert scope. (The cells in the background are mouse fibroblast cells. Only the colony in the centre are human embryonic stem cells) Credit: Ryddragyn/ Wikipedia

Research by Kai Jiao, M.D., Ph.D., and colleagues at the University of Alabama at Birmingham and in Germany has yielded fundamental insights into the causes of severe birth defects known as CHARGE syndrome cases. These congenital birth defects include severe and life-threatening heart malformations.

The researchers successfully inactivated the gene for CHD7 in the of mouse embryos, and then rigorously probed how this change in developing cardiac neural crest cells caused severe defects in the outflow tract and great arteries, leading to perinatal lethality. The heart defects in the embryos, and other birth defects, resembled human CHARGE syndrome defects. Human mutations in CHD7 are known to cause about 70 percent of CHARGE syndrome cases.

The study in Proceedings of the National Academy of Sciences, led by Jiao, co-corresponding author Karim Bouazoune, Ph.D., Philipps Universität Marburg, Marburg, Germany, and first author Shun Yan, Ph.D., a researcher V in Jiao’s lab, also clarifies a longstanding controversy. Previous attempts by others to alter CHD7 function in neural crest cells had failed to cause heart defects in several mouse models. This study’s improvement was use of better molecular scissors to delete a portion of the CHD7 gene.

A surprising finding in the current research was discovery of a new epigenetic function for CHD7, in addition to its well-established ATP-dependent chromatin remodeling activity. Chromatin is a DNA-protein complex consisting of the mammalian genome tightly wound around to create a string of nucleosomes, like pearls on a necklace. Chromatin remodeling factors like CHD7 use the energy of ATP to remodel the chromatin, making selected genes available for expression. The turning-on and turning-off of select sets of genes is fundamental to , during the time that a single fertilized egg grows into a complex fetus with at least 200 different types of cells, all originating from the same DNA genome, but differentiated using different gene programs.

In addition to the chromatin remodeling activity, Jiao and colleagues discovered that CHD7 acts in an ATP-independent fashion to recruit histone-modifying enzymes to target promoter or enhancer loci on the genome.

“Our findings strongly suggest that CHD7 can also directly recruit an H3K4 methyltransferase writer to target elements,” said Jiao, a professor in the UAB Department of Genetics. “The dual activities of CHD7 may represent an efficient mechanism to coordinate nucleosome remodeling and H3K4 methylation at these target loci. The mutual interaction between the CHD7 nucleosome remodeler and histone methylation machinery could form a positive feedback loop to stabilize epigenetic states at target elements.”

In other key findings of the study—in addition to showing an essential cell-autonomous role for CHD7 to regulate cardiac neural crest cell development—the researchers showed that a single point mutation in the CHD7 gene was sufficient to cause severe developmental defects and embryonic lethality in mammals. The researchers also used transcriptomic analyses to show that CHD7 fine-tunes the expression of a gene network critical for cardiac neural crest cell development. They followed that with a protein-protein interaction screen and found that CHD7 directly interacted with multiple developmental disorder-mutated proteins. One of these was WDR5, a core component of H3K4 methyltransferase complexes. That interaction with WDR5 led to the discovery of CHD7’s ability to recruit histone-modifying enzymes to target promoter or enhancer loci on the genome.

The researchers say that the CHD7 protein interactome suggests CHD7 is likely implicated in an even wider range of physiological processes and human diseases than previously anticipated.

“Importantly,” Jiao said, “we now provide a molecular framework of direct candidate interactors to investigate known or new CHD7 functions, as well as the molecular etiology of CHD7-associated diseases or phenotypes.”

The discovery of two different functions for CHD7 also could have clinical relevance. “Our data imply that patients carrying a premature stop codon versus missense mutations will likely display different molecular alterations,” Jiao said. “These patients might therefore require personalized therapeutic interventions.”

More information:
Shun Yan et al, CHD7 regulates cardiovascular development through ATP-dependent and -independent activities, Proceedings of the National Academy of Sciences (2020). DOI: 10.1073/pnas.2005222117

New activity found for CHD7, a protein factor vital in embryonic development (2020, December 3)
retrieved 3 December 2020
from https://p

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