Monstrous People > Mutants, clones and cyborgs

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onishadowolf:
I thought I would start this thread and sticky it here. Any one who comes across a fascinating read post it here. And if you can please site it.




Science Daily (May 31, 2009) MIT and Boston University engineers have designed cells that can count and "remember" cellular events, using simple circuits in which a series of genes are activated in a specific order.
Integrated circuits.
Such circuits, which mimic those found on computer chips, could be used to count the number of times a cell divides, or to study a sequence of developmental stages. They could also serve as biosensors that count exposures to different toxins.
The team developed two types of cellular counters, both described in the May 29 issue of Science. Though the cellular circuits resemble computer circuits, the researchers are not trying to create tiny living computers.
"I don't think computational circuits in biology will ever match what we can do with a computer," said Timothy Lu, a graduate student in the Harvard-MIT Division of Health Sciences and Technology (HST) and one of two lead authors of the paper.
Performing very elaborate computing inside cells would be extremely difficult because living cells are much harder to control than silicon chips. Instead, the researchers are focusing on designing small circuit components to accomplish specific tasks.
"Our goal is to build simple design tools that perform some aspect of cellular function," said Lu.
Ari Friedland, a graduate student at Boston University, is also a lead author of the Science paper. Other authors are Xiao Wang, postdoctoral associate at BU; David Shi, BU undergraduate; George Church, faculty member at Harvard Medical School and HST; and James Collins, professor of biomedical engineering at BU.
Learning to count
To demonstrate their concept, the team built circuits that count up to three cellular events, but in theory, the counters could go much higher.
The first counter, dubbed the RTC (Riboregulated Transcriptional Cascade) Counter, consists of a series of genes, each of which produces a protein that activates the next gene in the sequence.
With the first stimulus for example, an influx of sugar into the cell the cell produces the first protein in the sequence, an RNA polymerase (an enzyme that controls transcription of another gene). During the second influx, the first RNA polymerase initiates production of the second protein, a different RNA polymerase.
The number of steps in the sequence is, in theory, limited only by the number of distinct bacterial RNA polymerases. "Our goal is to use a library of these genes to create larger and larger cascades," said Lu.
The counter's timescale is minutes or hours, making it suitable for keeping track of cell divisions. Such a counter would be potentially useful in studies of aging.
The RTC Counter can be "reset" to start counting the same series over again, but it has no way to "remember" what it has counted. The team's second counter, called the DIC (DNA Invertase Cascade) Counter, can encode digital memory, storing a series of "bits" of information.
The process relies on an enzyme known as invertase, which chops out a specific section of double-stranded DNA, flips it over and re-inserts it, altering the sequence in a predictable way.
The DIC Counter consists of a series of DNA sequences. Each sequence includes a gene for a different invertase enzyme. When the first activation occurs, the first invertase gene is transcribed and assembled. It then binds the DNA and flips it over, ending its own transcription and setting up the gene for the second invertase to be transcribed next.
When the second stimulus is received, the cycle repeats: The second invertase is produced, then flips the DNA, setting up the third invertase gene for transcription. The output of the system can be determined when an output gene, such as the gene for green fluorescent protein, is inserted into the cascade and is produced after a certain number of inputs or by sequencing the cell's DNA.
This circuit could in theory go up to 100 steps (the number of different invertases that have been identified). Because it tracks a specific sequence of stimuli, such a counter could be useful for studying the unfolding of events that occur during embryonic development, said Lu.
Other potential applications include programming cells to act as environmental sensors for pollutants such as arsenic. Engineers would also be able to specify the length of time an input needs to be present to be counted, and the length of time that can fall between two inputs so they are counted as two events instead of one.
They could also design the cells to die after a certain number of cell divisions or night-day cycles.
"There's a lot of concern about engineered organisms if you put them in the environment, what will happen?" said Collins, who is also a Howard Hughes Medical Institute investigator. These counters "could serve as a programmed expiration date for engineered organisms."
The research was funded by the National Institute of Health Director's Pioneer Award Program, the National Science Foundation FIBR program, and the Howard Hughes Medical Institute.

onishadowolf:
ScienceDaily (Aug. 14, 2007) A major surprise emerging from genome sequencing projects is that humans have a comparable number of protein-coding genes as significantly less complex organisms such as the minute nematode worm Caenorhabditis elegans. Clearly something other than gene count is behind the genetic differences between simpler and more complex life forms.

Increased functional and cellular complexity can be explained, in large part, by how genes and the products of genes are regulated. A University of Toronto-led study published in the latest issue of Genome Biology reveals that a step in gene expression (referred to as alternative splicing) is more highly regulated in a cell and tissue-specific manner than previously appreciated and much of this additional regulation occurs in the nervous system. The alternative splicing step allows a single gene to specify multiple protein products by processing the RNA transcripts made from genes (which are translated to make protein).
"We are finding that a significant number of genes operating in the same biological processes and pathways are regulated by alternative splicing differently in nervous system tissues compared to other mammalian tissues," says lead investigator Professor Benjamin Blencowe of the Banting and Best Department of Medical Research and Centre for Cellular and Biomolecular Research (CCBR) at the University of Toronto.
According to Blencowe, it is particularly interesting that many of the genes have important and specific functions in the nervous system, including roles associated with memory and learning. However, in most cases the investigators working on these genes were not aware that their favorite genes are regulated at the level of splicing. Blencowe believes that the data his group has generated provides a valuable basis for understanding molecular mechanisms by which genes can function differently in different parts of the body.
Blencowe attributes these new findings in part to the power of a new tool that he, together with his colleagues including Profs. Brendan Frey (Department of Electrical and Computer Engineering) and Timothy Hughes (Banting and Best, CCBR), developed a few years ago. This tool, which comprises tailored designed microarrays or "gene chips" and computer algorithms, allows the simultaneous measurement of thousands of alternative splicing events in cells and tissues. "Until recently researchers studied splicing regulation on a gene by gene basis. Now we can obtain a picture of what is happening on a global scale, which provides a fascinating new perspective on how genes are regulated," Blencowe explains.
A challenge now is to figure out how the alternative splicing process is regulated in a cell and tissue-specific manner. In their new paper in Genome Biology, Dr. Yoseph Barash, a postdoctoral fellow working jointly with Blencowe and Frey, has provided what is likely part of the answer. By applying computational methods to the gene chip data generated by Matthew Fagnani (an MSc student) and other members of the Blencowe lab, Barash has uncovered what appears to be part of a "regulatory code" that controls alternative splicing patterns in the brain.
One outcome of these new studies is that the alternative splicing process appears to provide a largely separate layer of gene regulation that works in parallel with other important steps in gene regulation. "The number of genes and coordinated regulatory events involved in specifying cell and tissue type characteristics appear to be considerably more extensive than appreciated in previous studies," says Blencowe. "These findings also have implications for understanding human diseases such as cancers, since we can anticipate a more extensive role for altered regulation of splicing events that similarly went unnoticed due to the lack of the appropriate technology allowing their detection."
Blencowe's research is funded by grants from the Canadian Institutes of Health Research, the National Cancer Institute of Canada, and by Genome Canada through the Ontario Genomics Institute.
Co-authors of the study are: Matthew Fagnani, Yoseph Barash, Joanna Ip, Christine Misquitta, Qun Pan, Arneet Saltzman, Ofer Shai, Leo Lee, Aviad Rozenhek, Naveed Mohammad, Sandrine Willaime-Morawek, Tomas Babak, Wen Zhang, Timothy Hughes, Derek van der Kooy, Brendan Frey and Benjamin Blencowe.

onishadowolf:
ScienceDaily (May 25, 2009) Scientists at Oxford University have tamed a virus so that it attacks and destroys cancer cells but does not harm healthy cells.  They determined how to produce replication-competent viruses with key toxicities removed, providing a new platform for development of improved cancer treatments and better vaccines for a broad range of viral diseases.

Cellular microRNA molecules regulate the stability of mRNA in different cell types, and this newly-understood mechanism provides the possibility to engineer viruses for cell-specific inactivation. Cancer Research UK scientists at the University of Oxford, United Kingdom, with support from colleagues at Vrije Universiteit, Amsterdam, report that this approach can be used to regulate proliferation of adenovirus.
Adenovirus is a DNA virus widely used in cancer therapy but which causes hepatic disease in mice. Professor Len Seymour and colleagues found that introducing sites into the virus genome that are recognized by microRNA 122 leads to hepatic degradation of important viral mRNA, thereby diminishing the virus' ability to adversely affect the liver, while maintaining its ability to replicate in and kill tumor cells.
Tumor-killing replicating viruses are a hot topic in the biotherapeutics arena, with many clinical trials ongoing worldwide. That Professor Seymour's group set out to and has now defined a mechanism whereby wild type virus potency could be maintained in tumor cells but the virus could be 'turned off' in tissues vulnerable to pathology adds important information to the current base of knowledge.
"This approach is surprisingly effective and quite versatile. It could find a range of applications in controlling the activity of therapeutic viruses, both for cancer research and also to engineer a new generation of conditionally-replicating vaccines, where the vaccine pathogen is disabled in its primary sites of toxicity," Professor Seymour says.
The present study was intended mainly to explore and demonstrate the potential of this new mechanism to regulate virus activity. Although the current tumor-killing virus is useful in mice, transfer of the technology into the clinical setting will require re-engineering of the virus to overcome virus pathologies seen in humans, and it will be at least two years before this can be tested in the clinics.
Modified naturally-occurring viruses have already had important uses in medicine including their use as vaccines, notably for measles, mumps, polio, influenza, and chicken pox. They have already been developed as potential cancer-killing therapies, in an approach called virotherapy.
RC and FC are supported by Cancer Research UK; HC by a research studentship from the New Zealand Government, and MB by a Bellhouse Foundation Fellowship (Magdalen College, Oxford). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript. The authors have declared that no competing interests exist.
Journal reference:
Ryan Cawood, Hannah H. Chen, Fionnadh Carroll, Miriam Bazan-Peregrino, Nico van Rooijen, Leonard W. Seymour. Use of Tissue-Specific MicroRNA to Control Pathology of Wild-Type Adenovirus without Attenuation of Its Ability to Kill Cancer Cells.







I'm going to have to find shorter summaries.

oldbill4823:
Makes it all sound so easy.
Ok this really is incredible stuff that they are doing, truly amazing!

I am astounded though that here we are engineering and training genes to disable specific cancer cells, yet at the same time we are failing as a species in the most simple areas of life, ie overpopulation and energy demands.

Can we have some scientists involved in social engineering and training please.

Moloch:

--- Quote from: oldbill4823 on May 31, 2009, 04:11:42 AM ---Makes it all sound so easy.
Ok this really is incredible stuff that they are doing, truly amazing!

I am astounded though that here we are engineering and training genes to disable specific cancer cells, yet at the same time we are failing as a species in the most simple areas of life, ie overpopulation and energy demands.

Can we have some scientists involved in social engineering and training please.

--- End quote ---

First, that failure is more profound than you have stated, OB1. Here we are, striving to prolong the lives of individuals, when we already have nearly seven Billion of them, and more being born every day.

As for the folks to work on social engineering, we already have that. You can thank them for the current sorry state of affairs we're in now; where people fear death so much that they are willing to take a little bit more than they should - just to be able to keep going for a few more years.

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