Microbiology

Category: Microbiology

A robust, broad spectrum antibiotic, and a gene that confers immunity to that antibiotic are both found in the bacterium Staphylococcus epidermidis Strain 115. The antibiotic, a member of the thiopeptide family of antibiotics, is not in widespread use, partly due to its complex structure, but the investigators, from Brigham Young University, Provo, Utah, now report that the mechanism of synthesis is surprisingly simple. "We hope to come up with innovative processes for large-scale production and derivitization so that new, and possibly more potent versions of the antibiotic can become available, says co-corresponding author Joel S. Griffitts. The research is published ahead of print in Journal of Bacteriology.

As the threat of antibiotic resistance grows, scientists are turning to the human body and the trillion or so bacteria that have colonized us — collectively called our microbiota — for new clues to fighting microbial infections. They've logged an early success with the discovery of a new antibiotic candidate from vaginal bacteria, reports Chemical & Engineering News (C&EN), the weekly newsmagazine of the American Chemical Society.

MicrobiologySeptember 15, 2014 05:20 PM


This is a ribbon diagram showing the tertiary structure with secondary-structure elements identified and labeled.
The current Ebola virus outbreak in West Africa, which has claimed more than 2000 lives, has highlighted the need for a deeper understanding of the molecular biology of the virus that could be critical in the development of vaccines or antiviral drugs to treat or prevent Ebola hemorrhagic fever. Now, a team at the University of Virginia (UVA), USA – under the leadership of Dr Dan Engel, a virologist, and Dr Zygmunt Derewenda, a structural biologist – has obtained the crystal structure of a key protein involved in Ebola virus replication, the C-terminal domain of the Zaire Ebola virus nucleoprotein (NP) [Dziubanska et al. (2014). Acta Cryst. D70, 2420-2429; doi:10.1107/S1399004714014710].

For multicellular life—plants and animals—to thrive in the oceans, there must be enough dissolved oxygen in the water. In certain coastal areas, extreme oxygen-starvation produces "dead zones" that decimate marine fisheries and destroy food web structure. As dissolved oxygen levels decline, energy is increasingly diverted away from multicellular life into microbial community metabolism resulting in impacts on the ecology and biogeochemistry of the ocean.

In contrast to their negative reputation as disease causing agents, some viruses can perform crucial biological and evolutionary functions that help to shape the world we live in today, according to a new report by the American Academy of Microbiology.

MicrobiologyJuly 16, 2014 06:37 PM

Scientists have discovered a new pathway the dengue virus takes to suppress the human immune system. This new knowledge deepens our understanding of the virus and could contribute to the development of more effective therapeutics.

Like human societies--think New York City--bacterial colonies have immense diversity among their inhabitants, often generated in the absence of specific selection pressures, according to a paper published ahead of print in the Journal of Bacteriology.

Trillions of bacteria live in and on the human body; a few species can make us sick, but many others keep us healthy by boosting digestion and preventing inflammation. Although there's plenty of evidence that these microbes play a collective role in human health, we still know very little about most of the individual bacterial species that make up these communities. Employing the use of a specially designed glass chip with tiny compartments, Caltech researchers now provide a way to target and grow specific microbes from the human gut—a key step in understanding which bacteria are helpful to human health and which are harmful.


This image shows cross-sections of the empty prohead of the bacteriophage phi29 (left) and the fully assembled virus (right). A molecular motor transports the DNA (red) into the prohead through...
Researchers at the University of California, San Diego have found that DNA packs more easily into the tight confines of a virus when given a chance to relax, they report in a pair of papers to be published in in the early edition of the Proceedings of the National Academy of Sciences the week of May 26 and the May 30 issue of Physical Review Letters.

Using genome sequencing, National Institutes of Health (NIH) scientists and their colleagues have tracked the evolution of the antibiotic-resistant bacterium Klebsiella pneumoniae sequence type 258 (ST258), an important agent of hospital-acquired infections. While researchers had previously thought that ST258 K. pneumoniae strains spread from a single ancestor, the NIH team showed that the strains arose from at least two different lineages. The investigators also found that the key difference between the two groups lies in the genes involved in production of the bacterium's outer coat, the primary region that interacts with the human immune system. Their results, which appear online in Proceedings of the National Academy of Sciences, promise to help guide the development of new strategies to diagnose, prevent and treat this emerging public health threat.

MicrobiologyMarch 12, 2014 04:24 PM


Dr. David Coil, a microbiologist at UC Davis and Project MERCCURI team member, gathers microbial samples from the Sacramento Kings basketball court in the Sleep Train Arena.
Microbes collected from Northern California and throughout the nation will soon blast into orbit for research and a microgravity growth competition on the International Space Station (ISS).

The gut microbiota contains a vast number of microorganisms from all three domains of life, including bacteria, archaea and fungi, as well as viruses. These interact in a complex way to contribute towards both health and the development of disease — interactions that are only now being elucidated thanks to the application of advanced DNA sequencing technology in this field.

With antibiotic resistant infections on the rise and a scarce pipeline of novel drugs to combat them, researchers at the Los Angeles Biomedical Research Institute at Harbor-UCLA Medical Center (LA BioMed) are pursuing entirely new approaches to meet the challenge of drug-resistant infections by taming microbes rather than killing them.


In blue are Plasmodium falciparum malaria parasites in the sexual, gametocyte stage of development. In red are uninfected red blood cells.
Two teams have independently discovered that a single regulatory protein acts as the master genetic switch that triggers the development of male and female sexual forms (termed gametocytes) of the malaria parasite, solving a long-standing mystery in parasite biology with important implications for human health. The protein, AP2-G, is necessary for activating a set of genes that initiate the development of gametocytes -- the only forms that are infectious to mosquitos. The research also gives important clues for identifying the underlying mechanisms that control this developmental fate, determining whether or not a malaria parasite will be able to transmit the disease.


How dengue virus enters cells of our immune system: a 3D projection of a cell expressing on its surface DC-SIGN (stained in blue with antibodies) that have captured many dengue viruses (in green or green combined with red) and internalized dengue viruses (shown only in red).
Dengue fever, an infectious tropical disease caused by a mosquito-borne virus, afflicts millions of people each year, causing fever, headache, muscle and joint pains and a characteristic skin rash. In some people the disease progresses to a severe, often fatal, form known as dengue hemorrhagic fever. Despite its heavy toll, the prevention and clinical treatment of dengue infection has been a "dramatic failure in public health compared to other infectious diseases like HIV," said Ping Liu of the University of North Carolina at Chapel Hill.


Some smaller molecules (such as the Lactone in the middle) are able to destruct the arrangement of the amino acids required for the cohesion of the subunits of the bacterial protease ClpP. As a result the protease breaks into two parts, which are completely inactive. This approach massively disturbs the metabolism of the bacterium, giving the immune system time to react. And, because the bacterium isn't killed, the development of new resistances can be avoided.
Proteins are made up of a chain of amino acids and are vital for all cell processes. Proteases are among the most important types of protein. Like "molecular scissors", they cut other proteins at given positions and thereby execute important cell functions. By cutting the amino acid chains to the right length or breaking proteins apart they, for example, activate or deactivate proteins, decompose defective ones or switch signal sequences that serve to transport proteins to their proper position within a cell.

The hepatitis C virus (HCV) has a previously unrecognized tactic to outwit antiviral responses and sustain a long-term infection. It also turns out that some people are genetically equipped with a strong countermeasure to the virus' attempt to weaken the attack on it.


North Carolina State University researchers have developed a technique to selectively kill specific strains of bacteria.
Researchers from North Carolina State University have developed a de facto antibiotic "smart bomb" that can identify specific strains of bacteria and sever their DNA, eliminating the infection. The technique offers a potential approach to treat infections by multi-drug resistant bacteria.

The Annals of the American Thoracic Society has released a comprehensive supplement on the 56th annual Thomas L. Petty Aspen Lung Conference entitled "The Lung Microbiome: A New Frontier in Pulmonary Medicine."

Innovative work by two Florida State University scientists that shows the structural and DNA breakdown of a bacteria-invading virus is being featured on the cover of the February issue of the journal Virology.


Macrophage (in red) infected with fluorescent labelled E. coli (in yellow or blue).

Bacteria can evolve rapidly to adapt to environmental change. Bacteria can evolve rapidly to adapt to environmental change. When the "environment" is the immune response of an infected host, this evolution can turn harmless bacteria into life-threatening pathogens. A study published on December 12 in PLOS Pathogens provides insight into how this happens.


Life cycle of the human malaria parasite.
Say "malaria" and most people think "mosquito," but the buzzing, biting insect is merely the messenger, delivering the Plasmodium parasites that sickened more than 200 million people globally in 2010 and killed about 660,000. Worse, the parasite is showing resistance to artemisinin, the most effective drug for treating infected people.

Around 20 percent of all humans are persistently colonized with Staphylococcus aureus bacteria, a leading cause of skin infections and one of the major sources of hospital-acquired infections, including the antibiotic-resistant strain MRSA.

In a pair of landmark studies that exploit the genetic sequencing of the "missing link" cold virus, rhinovirus C, scientists at the University of Wisconsin-Madison have constructed a three-dimensional model of the pathogen that shows why there is no cure yet for the common cold.

The medical, humanitarian and economical impact of viral diseases is devastating to humans and livestock. There are no adequate therapies available against most viral diseases, largely because the mechanisms by which viruses infect cells are poorly known. An interdisciplinary team of researchers from the University of Zurich headed by cell biologist Prof. Urs Greber now presents a method that can be used to display viral DNA in host cells at single-molecule resolution. The method gives unexpected insights into the distribution of viral DNA in cells, and the reaction of cells to viral DNA.

Researchers at Lund University in Sweden have for the first time managed to measure the internal pressure that enables the herpes virus to infect cells in the human body. The discovery paves the way for the development of new medicines to combat viral infections. The results indicate good chances to stop herpes infections in the future.


This is the cover of the American Journal of Botany September issue featuring the Rhizosphere Interactions special section.
We often ignore what we cannot see, and yet organisms below the soil's surface play a vital role in plant functions and ecosystem well-being. These microbes can influence a plant's genetic structure, its health, and its interactions with other plants. A new series of articles in a Special Section in the American Journal of Botany on Rhizosphere Interactions: The Root Microbiome explores how root microbiomes influence plants across multiple scales—from cellular, bacterial, and whole plant levels to community and ecosystem levels.

Researchers have found that apoptosis, a natural process of programmed cell death, can reactivate latent herpesviruses in the dying cell. The results of their research, which could have broad clinical significance since many cancer chemotherapies cause apoptosis, was published ahead of print in the Journal of Virology.

MicrobiologyAugust 19, 2013 05:40 PM

The human body is full of tiny microorganisms—hundreds to thousands of species of bacteria collectively called the microbiome, which are believed to contribute to a healthy existence. The gastrointestinal (GI) tract—and the colon in particular—is home to the largest concentration and highest diversity of bacterial species. But how do these organisms persist and thrive in a system that is constantly in flux due to foods and fluids moving through it? A team led by California Institute of Technology (Caltech) biologist Sarkis Mazmanian believes it has found the answer, at least in one common group of bacteria: a set of genes that promotes stable microbial colonization of the gut.

Every cell in an organism's body has the same copy of DNA, yet different cells do different things; for example, some function as brain cells, while others form muscle tissue. How can the same DNA make different things happen? A major step forward is being announced today that has implications for our understanding of many genetically-linked diseases, such as autism.

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