TALLER DE INGENIERIA GENETICAA

Tienes iteres en la ciencia , la ingeniería genética , la Biología Molecular ?si tu respuesta es SI , te invitamos al:
Segundo Taller de Ingeniería Genética.
UAQ-Campus Aeropuerto 
Diciembre 6 y 7 ,2012 .
informes :
Dr. Fausto Arellano 
talleringenieriagenetica@gmail.com
Unidad de Microbiología Básica y Aplicada

New insight into complexities of cell migration

September 20, 2012 by Katie Neith

Migrating cells in a nematode are identified and stained green in the top image. Looking closer, the glowing cell is extracted for analysis using a glass pipette. Credit: Caltech / Mihoko Kato (Phys.org)—At any given moment, millions of cells are on the move in the human body, typically on their way to aid in immune response, make repairs, or provide some other benefit to the structures around them. When the migration process goes wrong, however, the results can include tumor formation and metastatic cancer. Little has been known about how cell migration actually works, but now, with the help of some tiny worms, researchers at the California Institute of Technology (Caltech) have gained new insight into this highly complex task. Ads by Google Cell Signaling Technology - High-Quality Antibodies & Reagents for Signaling Pathway Research - www.CellSignal.com The team's findings are outlined this week online in the early edition of the Proceedings of the National Academy of Sciences (PNAS). "In terms of cancer, we know how to find primary tumors and we know when they're metastatic, but we're missing information on the period in between when cells are crawling around, hanging out, and doing who knows what that leads to both of these types of diseases," says Paul Sternberg, Thomas Hunt Morgan Professor of Biology at Caltech, and corresponding author of the paper. To learn more about those crawling, or migrating, cells, Sternberg looked at the animal he knows best—the tiny Caenorhabditis elegans, a common species of roundworm that he has been studying for many years. Despite their small size, the worms actually share quite a few genes with humans.  "Migration is such a conserved process," says Mihoko Kato, a senior research fellow in biology at Caltech and a coauthor of the paper. "So whether it happens in C. elegans or in mammals, like humans, we think that many of the same genes are going to be involved." Contained in each cell—be it human or worm—are thousands of genes, all of which have a special job, or jobs, to do. Of these genes, roughly one-third are active in a given cell. To see what genes are expressed during migration, Sternberg and Kato, along with Erich Schwarz, a research fellow in Sternberg's lab, studied a single cell, called the linker cell (LC), in the worms; during reproductive development, LCs travel almost the entire length of the worm's body. Using high-powered microscopy, the team identified LCs at two intervals, 12 hours apart, during the worm's larval stage, and removed them from the animals. Then, using sequencing and computational analysis, they determined the genes that were actively expressed at these two migration time points. This method of study is called transcriptional profiling. Ads by Google Real-Time Supermixes for - Dye or Probe Based qPCR. Sensitive, Efficient and Robust. By Bio-Rad. - www.bio-rad.com "By understanding the normal migration of a single cell, we can understand something about how the cells are programmed to navigate their environment," says Sternberg, who is also an investigator with the Howard Hughes Medical Institute. "Our view of cancer metastasis is that the tumor cells confront some obstacle and then they have to evolve to get through or around that obstacle. The way they probably do that is by using some aspect of the normal program that exists somewhere in the genome." He says that learning more about different ways that cells migrate may lead to the development of new types of drugs that block this process by targeting specific genes. The team plans additional transcriptional profiling studies to obtain more detailed information about the functions of particular C. elegans genes involved in migration—and, eventually, of similar genes in higher organisms, including humans. "We selected genes present in both worms and humans, but which have not been studied much before us," says Schwarz. "Since we found that some of these genes help worm LCs migrate, we think each one may have a related human gene helping cells migrate, too." "The nice thing about this technology is that you can use it with any cell type," adds Kato, who points out that their studies have already helped identify new functions for known genes possessed by both the worms and humans. "It's a similar process to do transcriptome profiling using human cells." In addition to identifying drug targets, the team is also hoping to find a good signature, or molecular marker, for migrating cells. "This kind of information could be very useful diagnostically, to help identify cells that are doing things that they shouldn't be doing, or weird combinations of genes that shouldn't be expressed together, which is what a tumor cell might have," says Sternberg. "This work lays the foundation for really understanding what information is critically needed from mammalian cells for tumor cells to be able to migrate." The study is titled, "Functional transcriptomics of a migrating cell in Caenorhabditis elegans."

Zachary Copfer Blends Bacteria And Photography In Bacteriography Series (PHOTOS, VIDEO)

http://www.huffingtonpost.com/2012/09/18/zachary-copfer-blends-bac_n_1889677.html?utm_hp_ref=arts

simposio MICROBIOLOGIA

simposio de microbiologia COORDIALMENTE INVITADOSSS ... :) http://aeropuerto.uaq.mx/convocatorias/pdf/1er_Simposio1.pdf

LINK. PARA SABER LA SECUENCIA DE TU BACTERIA DE INTERES :)

http://www.ncbi.nlm.nih.gov/sites/entrez?db=genome

INVESTIGACION DE CLAMIDIA

This electron micrograph shows the flower-like structure of polymorphic membrane protein D (PmpD) after it was purified from the surface of the C. trachomatis bacterium. Scientists are hoping to develop PmpD into a vaccine candidate to prevent chlamydial infection. Credit: NIAID

NIAID Researchers Developing Vaccine for Chlamydia

The bacterium Chlamydia trachomatis is among the oldest and most prevalent causes of infectious disease on earth. The World Health Organization (WHO) estimates that between 80 and 140 million people are infected with C. trachomatis, mostly women and children in developing countries, making chlamydia the most common bacterial disease in the world. In the United States, chlamydia is perceived primarily as a “silent” disease that, despite showing no symptoms in more than half of the infected population, can damage reproductive organs and cause infertility. Chlamydia is the most reported sexually transmitted disease in the United States, and, in 2006, U.S. cases for the first time topped 1 million, according to the Centers for Disease Control and Prevention (CDC).
But in more than 50 developing countries, C. trachomatis is known for causing blindness. WHO estimates that untreated cases of the disease trachoma have left about 6 million people blind in Africa, the Middle East, Central and Southeast Asia, and Latin America. Trachoma causes eyelids to fold inward, so that the eyelashes rub the eyeball and scar the cornea, which can result in impaired vision and blindness.
In 1997, WHO coordinated a multinational program to eliminate blinding trachoma by 2020, called Global Elimination of Trachoma (GET2020). Because chlamydia is easily treated and cured with medical care, GET2020 has highlighted four areas for eliminating trachoma: eyelid surgery, facial cleanliness, environmental changes, and antibiotics.
Another focus of the WHO effort is to develop a vaccine to prevent chlamydial infection. One of the greatest challenges to fighting chlamydial infection is that people do not develop a sustained protective immune response to the infection. Understanding how C. trachomatis evades host immunity is central to developing a vaccine. That’s where NIAID scientists hope to contribute.

A Promising Re-Start

In 1975, Harlan Caldwell, Ph.D., now chief of NIAID’s Laboratory of Intracellular Parasites, was a graduate student at the University of Washington. He observed that blood samples from people who suffered different chlamydial diseases all appeared to have antibodies against the same protein antigen from C. trachomatis. He suspected that the antigen played a key role in the spread of disease, but at that time there was no equipment to further study the hypothesis.
The materials went into the freezer until, some 30 years later, while conferring with a colleague about C. trachomatis surface proteins, Dr. Caldwell recalled the earlier work. He had an idea of how to use new technology to study its potential to prevent C. trachomatis from spreading.
Now, based on successful initial laboratory test results, NIAID has sought patent protection on the concept, and Dr. Caldwell’s research group has begun to study animal models. But much work remains to be done to understand how C. trachomatis spreads and evades human immunity.

Deconstructing PmpD

Dr. Caldwell’s group is trying to confirm that the protein antigen he identified, known as polymorphic membrane protein D, or PmpD, has an active role in suppressing an immune response. That information could become the basis for a multivalent vaccine, or a vaccine that prevents infection from all 15 varieties of C. trachomatis. If PmpD indeed suppresses host immunity, then a vaccine that neutralizes PmpD could prevent infection and allow protective immunity to develop.
In its latest work, published online November 10, 2008, in Infection and Immunity, the group observed structural details of PmpD, showing that it exists in two forms that could each promote infection. Though they do not know the precise mechanisms involved, the scientists hypothesize that one form, found on the cell surface, is a flower-like structure that could help the bacteria attach to host cells and invade them. The other form is soluble; the scientists suggest its fragments could be released into the environment around a cell, where they act on and suppress cells involved in the immune response.
Understanding how these forms of PmpD function is critical to the design of a vaccine. Ultimately, as their work advances, Dr. Caldwell’s group will be trying to learn whether a PmpD-based vaccine can generate multi-functional, neutralizing antibodies that can block C. trachomatis infection.