Dirty Fingertips May Leave Forensic Clue

As we all know, bacteria are found practically anywhere including our hands and the things that we touch. A study published in March 2010 by Noah Fierer and his team suggests that bacteria from a person’s hands could one day be used to accurately identify that individual. If this is true, we will be able to track down criminals who remove their fingerprints and/or leave no DNA evidences (such as saliva, tissue, blood, or semen) from the bacteria trail they leave on the objects they touch. Fierer says that a human hand can contain up to 100 different species of bacteria and only ~13% of the same makeup is shared between any two individuals.

Fierer and colleagues did a test to see whether bacteria on an object are more similar to the bacteria found on the owner’s skin than to bacteria on the general population. They compared bacteria sequences found on 9 computer mice to bacteria collected from the hands of 270 individuals. The results suggest that bacteria from each mouse closely matched those from the owner’s hands. Fierer says that this technique was 70% - 90% accurate overall but the percentage could increase as the technology becomes more sophisticated.

Although this intervention attracts many interests, there are limitations of this technology. For example, a professor from Stanford University, David A. Relman, says that it isn’t possible yet to separate mixed-up bacterial trails when more than one person touches the same object. Also, there could be changes to the distribution of bacteria once they left the human hand, thus making it harder to link the microbes to a person.

Personally, I think DNA evidences are more reliable than this technique especially since we already have a large database which we can use to crosscheck the DNA we find on a crime scene. The bacterial trails technique, in the other hand, requires us to have a sample from the suspect whom may not be identified yet.




Fierer, N., Lauber, C. L., Zhou, N., McDonald, D., Costello, E. K., & Knight, R. (2010). Forensic identification using skin bacterial communities. PNAS , 6477-6481.
Khan, A. (2010, March 16). Bacterial trail may be next forensic clue. Retrieved May 26, 2010, from LA Times: http://www.latimes.com/news/science/la-sci-bacteria16-2010mar16,0,5990278.story

Horizontal Gene Transfer in Higher Eukaroyotes

A Role for Host–parasite Interactions in the Horizontal Transfer of Transposons Across Phyla

http://www.nature.com/nature/journal/v464/n7293/abs/nature08939.html

Horizontal gene transfer is a process that geneticists have mostly studied in bacteria, and is offered as a possible explanation to how bacteria are able to quickly become antibiotic resistant. But only recently has this same process been documented in higher organisms, thanks to the work Gilbert et al. The findings in this article pose an interesting question: do higher organisms transfer genes to other species more often than originally thought?

Simply put, this article argues that there is a type of parasitic blood-sucking bug that feasts on tetrapods in many different phylas, and is causing horizontal gene transfer (HGT). Although we haven’t gone over this extensively in class, many of us have heard about HGT in other classes we have taken. In HGT, an organism incorporates genetic material to another organism without being the offspring or a mate of that organism. This phenomenon is noted mostly in unicellular organisms, and so I found it really interesting that this bug could inflict HGT on animals of higher complexity.

The authors of the article uses a few different phylogenies to show how the animals affected by the mites are not closely related and are from different regions of the world, and therefore should not have too much similar DNA. To give an idea, some of the animals included are opossums, squirrel monkeys, frogs, lizards, and chickens. Then, from these dispersed animals, the researchers sequenced genomes and found a portion of genes shared amongst all of the animals and the mites. They therefore concluded that this is proof of HGT within these phyla. HGT mechanisms are still not clearly understood, and so how genes are transferred is not specifically talked about in this paper. Because of this and the fact that there may be other factors causing similar sequences (such as unknown distant relatives), I’m not really sure if I believe this paper or not. It seems too far-fetched that the authors randomly chose species and they all had the sequences in common with the mite. I feel like there is a lot missing from the article, and I would like to see data on animals that are more closely related to all of the species. I feel like I need proof that related species to the ones in the study who are not parasitized by the bug do not also have the same sequence. If I saw this data, I might be more inclined to believe that HGT can be caused by a parasitic bug across many multicellular phyla. All in all, this article leaves me wanting more information on just how common HGT is in higher organisms and it will surely be interesting to learn.

Clement Gilbert1*, Sarah Schaack1*, John K. Pace II1, Paul J. Brindley2 & Cedric Feschotte1

“A role for host–parasite interactions in the horizontal transfer of transposons across phyla”

Nature Vol 464 April 2010 (p 1347-1352)

Forensic Analysis of DNA

An article in the May edition of Scientific America, entitled Portrait in DNA, discusses the possibility of using DNA to create police style sketches of criminals. This seems to be possible considering scientists recently published a sketch (pictured above) of a 4000 year old ancient Greenlander drawn solely from his DNA remains. All the DNA used came from a small clump of hairs that had been preserved in the permafrost! The scientists first determined that the man was of North Asian decent based on a pattern of DNA variations most commonly found in Siberian populations. They then interpreted single nucleotide polymorphisms (SNPs) in four genes linked to brown eye color in modern Asians. They also found SNPs associated with shovel-shaped front teeth, dry ear wax, and dark skin. They also found variations typical in populations that have adapted to cold indicating that the man had ample body fat. Using this type of analysis of criminal DNA would greatly help investigators find the criminals, especially when there are no witnesses to give a description to an artist. Scientists at George Washington are in the process of developing forensic kits that would determine the subjects eye and hair color, sex and ancestry. However age is difficult to determine because although scientists could took at telomeres, the chromosomal ends that shrink with time, there are many health and environmental factors that influence shrinkage.
The ancient Greenlander was also identified as having a high risk for hypertension and diabetes. Some scientists worry about the ethics behind announcing such discoveries about a criminal to the world, for example the fact that the criminal has a high likelihood of being obese, a smoker, an alcoholic or depressed. Clearly medical privacy is an issue here but if this technology could help us find killers, isn't it worth it? I do hope that a forensic kit as mentioned would only be released and used once it was completely reliable. Unreliable information about physical appearance of the a criminal would only hinder the investigators job.
Tiffany Flossman

Ventor's Work

Dr. J. Craig Venter is founder of J. Craig Venter Institute and Celera Genomics, the latter having sequenced the first complete human genome as well as the fruit fly, mouse and rat genome. A leading connoisseur in the field of genetics, Dr. Venter has been described as a trail blazer and genome pioneer and has been awarded numerous prestigious scientific awards. Though obviously an important and highly intellectual individual, Dr. Venter was perhaps a bit too haste in his description of his latest achievement- a ‘synthetic cell’.

A team of scientists led by Daniel G. Gibson, Hamilton O. Smith and Dr. Venter published their recent findings in Science; they were able to synthesize an entire bacterial genome compromised of many 1,000 base-pair long DNA fragments. The original genome came from a bacterium infecting goats though was manufactured in a way that rendered it un-pathogenic. The 1,080,000 base-pair long genome was inserted into another species of bacterium and was able to create new protein and organelle not endemic to that cell. Dr. Venter and his team eventually hope to mass produce cells engineered to make specific types of proteins/chemicals in the hopes of making vaccines and biofuels. In fact, he currently is contracted with Exxon to ‘create’ algae using this current technique designed to produce certain chemicals in hopes of creating biofuels.

Though Dr. Venter’s achievement will help the scientific community, other scientists have polar opinions on the magnitude of his work. Gerald Joyce, a biologist at the Scripps Research Institute in La Jolla, California, praised Venter stating he has created a powerful tool. Another, David Baltimore, a geneticist at Caltech, has called Dr. Venter’s achievement what it is- a technical advancement, perhaps akin to making a really really long primer. In the truest sense of the word synthesizing a cell (in my opinion) would be creating all the components of a cell, not just the genome. Perhaps in the future journalists and Dr. Venter will use greater discretion when describing his scientific advancements, or maybe he will find a small bit of humility the next time he’s sailing his yacht.

Tetrad Analysis in Arabidopsis

Separation of Arabidopsis Pollen Tetrads is Regulated by QUARTET1, a Pectin Metylesterase Gene.

Kirk E. Francis, Sandy Y. Lam, and Gregory P. Copenhaver
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1630721/

For years, researchers have been studying a variety of model systems from C. elegans to Arabidopsis to even yeast spores.  How do scientists go about these studies, and how is it that research in the sciences is able to continue after a discovery has been made?  Researchers must continue searching for answers to questions that come up all over the place.  How do plants reproduce? How do humans process sugar?  Why can't some people process a certain food and others can? What is the cause of Down Syndrome?  Questions like these allow researchers to continually make new hypotheses for experiments.  Applying science to everyday life can prove challenging, but if one actually takes the time to think about it, the results can be more than excellent.

One area of popular research includes studying the model system plant, Arabidopsis thaliana.  The above link to this paper takes you to a detailed paper on the experiment and procedures used to discover the function of a gene in the Arabidopsis plants that functions in meiosis and reproduction in the plants.  However, this experiment is not just a regular study that went through and sequenced genes in the plant.  The researchers applied a method used normally in yeast, which relies on the analysis of their haploid spores.

This article describes how pollen tetrads are separated in Arabidopsis, and how the quartet gene regulates this function.  The authors go into detail about the studies they were able to do using tetrad analysis, including mapping the five different centromeres and distinguishing sporophytic and gametophytic mutants.  Analysis of these tetrads with both the wild type and different mutant combinations resulted in discovering how these genes (and other genes as well) play a crucial role in the proper development and release of mature pollen grains.  The authors also discuss the different phenotypes of each mutant and what process is affected in each mutant gene, such as a mutation in the qrt 1 gene results in proper depositing and degradation of a certain cell wall, but a failure to release the entire layer and thus a part of it remaining intact during meiosis.

This study is especially important because not only does it allow researchers to use a method used normally in yeast mutant analysis, but it allows for more research and development in such processes like meiosis, which are critical reproductive processes.  Studying and discovering functions of such genes like the qrt gene may even allow for research in such areas like food crop production that will result in more successful yields.  Being able to analyze the pollen grains from the Arabidopsis plants allowed researchers to not only analyze mutants affecting the meiotic processes or the plants, but also their reproductive abilities, as well as mapping out the locations of the different qrt genes they discussed.  Figure 2 is especially interesting because it specifically shows in detail the location of the qrt1 gene and its surrounding regions, identifying the wild type as well as the mutant sequences.  Such comparisons may allow for further research in this area, allowing researchers to see just how mutations can really affect a genome of an organism.
Studying tetrads in this particular experiment not only allowed researchers to present a new way of looking at the arabidopsis model system, but allowed for such studies to be conducted that allowed analysis of a mutation affecting a crucial biological process.  Since meiosis is so crucial to successful production of viable progeny, using tetrads provided a perfect way to directly view meiotic products and the effects of different mutations in the qrt gene leading to problems in proper segregation and meiosis.  This experiment is so important because it not only discusses a breakthrough method of mutant analysis in a different model system than yeast, but it allowed for the direct analysis of a mutation via its meiotic products.  Such a study like this will likely affect science later by providing insight in new studies of mutations in processes like meiosis, pollen production and plant reproduction, as well as the discovery of pathways involving genes involved in such processes like these.

Separation of Arabidopsis Pollen Tetrads Is Regulated by QUARTET1, a Pectin Methylesterase Gene

Kirk E. Francis, Sandy Y. Lam, and Gregory P. Copenhaver

Plant Physiol. 2006 November; 142(3): 1004–1013. doi: 10.1104/pp.106.085274.

PMCID: PMC1630721

Art and Statistical genomics

Art and Statistical genomics
I came upon this site by following my former graduate student Josh Mell's blog "No DNA control". Here is a link to the lab page for Chiara Sabatti, a Professor of Human Genetics and statistics at UCLA.  She integrates an appreciation of art and literature beautifully with an eye to the presentation of statistical data. It reminds me that you never stop thinking about science. One person's world is viewed through a prism that reflects the passion of his or her own work.What do these images remind you of?
 (see my comments below)

1. Unknown
2. Miro Souvenir de Montroig
3. Paul Klee-In the Current Six Thresholds, 1929 Oil and tempera on canvas, 17 1/8 x 17 1/8 inches
Solomon R. Guggenheim Museum

Solving the CRV puzzle

The study of copy number variations (CRVs) may soon revolutionize the understanding of hundreds of prevalent diseases. Though some genetic diseases have been mapped to specific genes in a specific chromosome location, many still are largely not understood. Many diseases such as mental illnesses, autism, obesity, and others are believed to have a significant genetic component; however scientists have been unable to definitively determine genetic contributions.
New discoveries regarding copy number variations may provide the answer. The concept of varying copies of genetic sequences has existed for some time. In the early 20th century, scientists came to understand that inheriting two copies of an allele can have vastly different effects than the inheritance of a single copy. Also, in the study of aneuploidy, the conclusion was reached that aberrant numbers of chromosome copies can cause significant phenotypic effects. In many cases, multiple gene copies results in over expression of the gene product, leading to possibly deleterious phonotypic effects. Many of these copy variations are responsible for disease.
In recent years, with the increasing availability and efficiency of genome sequencing technology, scientists have been surprised to find that large variation exists between individuals in the copy number of various genomic sequences. Based on previous knowledge, scientists suspect that many of these variations could be responsible for predisposition to a host of various diseases. With each study that is conducted, the estimate of copy number variations per individual rises. The current count is upwards of 60 CRV’s per person.
Continued studies have linked several prevailing diseases such as schizophrenia and Crohn’s disease to abnormal CRV’s in specific genomic regions. It is possible that one such CRV is not enough to cause the disease, but that the total effect of CRV’s in different locations along with other genetic and environmental factors could greatly increase the disease risk. Studies are currently being conducted to identify CRV’s as small as 500bp. Stephen Scherer, a prominent Canadian researcher, is one of the leaders in this area of study.
The future of CRV studies appears promising and may enable scientists to solve the puzzling mysteries of the cause and inheritance of many debilitating diseases.

Article from The Scientific American:
http://www.scientificamerican.com/article.cfm?id=too-little-too-much

More about Dr. Stephen Scherer, one of the leaders in this research:
http://www.tcag.ca/scherer/

The complementation test and its exceptions

In order to understand genetic interactions, one mechanism is to determine whether the two genes are in the same or different complementation groups. However, this can be tricky because there are exceptions to the rules.

This review summarizes the theory behind the complementation test and its applications by citing examples from working with C. elegans. The criteria for the complementation test are discussed: the mutations must be recessive, mutations that fail to complement can cause homozygous phenotypes, the heterozygote can express a more severe phenotype than either homozygote alone, and if the gene is in a complex locus, the mutation can affect more than one gene product. This article discusses complications with the complementation test where it is unreliable and in certain cases, may even be misleading by providing examples. One situation is when alleles of the same gene complement each other, defined as intragenic complementation. The author also provides examples of different ways in which mutant alleles that fail to complement can mutually correct each other by reducing the dosage of a mutant product, stabilizing a complex, or by providing the missing function. Another situation that may be misleading is when there is second-site non- complementation in which alleles in the same complementation groups behave as if they are alleles that are non- complementary by acting as poisons or by double-haplo-insufficiency. This article does a good job of providing examples of different scenarios that were covered in lecture.

The article goes into more detail about second-site non-complementation using mutations in the spe-6 gene of C. elegans as an example. Mutations in the spe-6 gene leads to MSP assembly defect, a cytoskeletal protein which provides motility for spermatozoa. This leads to sterility due to defective primary spermatocytes that do not form spermatids. Spe-6 mutant spermatocytes arrest meiosis at diakinesis and chromosomes fail to segregate to the metaphase plate resulting in spermatocytes with four half-spindles surrounding unsegregated chromosomes. All four spe-6 alleles plus a chromosome III deficiency that deletes the spe-6 gene fail to complement two small overlapping chromosome IV deficiencies, eDf18 and eDf19. The non-complementation can be expected if gene products coded byeDf18 and eDf19 are necessary with the spe-6 gene product to promote MSP assembly. Varkey and others tested all spe-6 alleles located on chromosome III against both deficiencies, eDf18 and eDf19 of chromosome IV. All the other alleles failed to complement either deficiency. However, the spe-6(hc143) allele complemented better than the others. Varkey then tested another deficiency of thespe-6 gene, eDf2(III), which deletes the entire spe-6 gene. Results indicated that it also failed to complement leading to the conclusions that the interaction between the spe-6 gene and the unlinked deficiencies is due to reduced dosage of hemizygous genes.

References :
Yook, K. Complementation (October 06, 2005), WormBook, ed. The C. elegans Research Community, WormBook, doi/10.1895/wormbook.1.24.1, http://www.wormbook.org.
http://www.ncbi.nlm.nih.gov/bookshelf/br.fcgi?book=wormbook&part=complementation
J. P. Varkey, P. L. Jansma, A. N. Minniti, and S. Ward. The Caenorhabditis Elegans Spe-6 Gene Is Required for Major Sperm Protein Assembly and Shows Second Site Non-Complemehttp://www.ncbi.nlm.nih.gov/pmc/articles/PMC1205300/?tool=pubmedntation with an Unlinked Deficiency. Genetics. 1993 January; 133(1): 79-86. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1205300/?tool=pubmed

Synthetic Life, Now Reality

20 May 2010

Dr. Craig Venter has created the world’s first synthetic life form.

An article published in Science today shows Dr. Venter and his team created a complete genome from scratch, using chemically synthesized fragments. These fragments can only be made to about 80bp long and as he describes are like legos; they have to piece them together to create the genome. The genome is based on an existing bacterium but has been altered so that it will only grow on super rich media. They did this to ensure containment. They also use “watermarks” to encode their names’ into the genome, to show that it is synthetic.

They then insert the synthetic genome into a cell. He describes the genome as the software of the cell. Once the cell has new software the cell will completely changes its processes and become whatever the software tells it to. Dr. Venter also talk about how this changes the way we think about life. Life is now shown to be dynamic. One day a cell is a bacteria the next its yeast.

He tells about the possible applications of this technology. We will be able to program cells to create biofuels or to make algae to absorb CO2 or create vaccines without the need of chicken eggs.

This break through is estimated to be worth trillions of dollars.

This article has a Skype interview with Dr. Venter:

http://www.sfgate.com/cgi-bin/blogs/ybenjamin/detail??blogid=150&entry_id=64058

You can find the research paper here:

http://www.guardian.co.uk/science/2010/may/20/creation-bacterial-cell-craig-venter


C. Venter et al., 20 May 2010, Sciencexpress

To Review or Not to Review?

Review: The Art and Design of Genetic Screens: Caenorhabditis elegans
Erik M. Jorgensen and Susan E. Mango
http:beadle.rutgers.edu/MMG/502files/502-Ce/C.%20elegans%20Screens%20nrg%202002.pdf


Despite the fact that all of the important breakthroughs in scientific research are published in very structured and often overly complex papers, I find that reviews are oftentimes even more enlightening. Rather than focusing on blowing away one's audience with a preponderance of field jargon and perfect sentence formatting and grammar, reviews do just that, review. They are great if you are new to a topic and need to get familiar with the vocabulary. Or maybe you are curious about some new concept you heard about on the news and want a brief but detailed overview. They can also be especially helpful as a study aide since they usually go over a topic from beginning to end, including discovery, experiments, uses, and the future. No matter what your motivation for reading a review, you will probably finish it with a broader and more well rounded understanding of a concept than you would have if you had read a detailed research paper. Not to mention that you might even get a few laughs out of it.

This article in particular is a great overview of the history and evolution of genetic research using C. elegans. Not only does it go over the history of this organism's use, but it also outlines what makes it such a great model organism and features a concise yet informative summary of C. elegans life cycle and morphology. In fact I found all of the figures and images to be especially clear and helpful. The box on EMS mutagenesis was particularly interesting since in my experience most papers or books seem to gloss over the details of how it is actually preformed. Understanding the details of the process a little better helps to emphasize why EMS is used so often in genetic analyses.

The bulk of the article goes over in depth the plethora of screens that are available to be condcuted for C. elegans. In a clever twist, the authors give a helpful analogy of screens from heaven, hell, and purgatory to underline the wide variety of screen and how applicable and usable they are. Several screens we have discussed in class are mentioned in detail, such as simple F2 screens with mutants of the same phenotype as well as selective screens (i.e. screens from heaven). Many other experiments are also discussed which we have not covered, such as microscope and laser ablation screens, large scale screen,s and modifier screens. While each of these screens has their own specific details and protocols, they all revolve around the same basic ideas we have discussed in class: looking for and analyzing the significance of certain mutants that result from various crosses or mutagenesis. The authors end the review with a lengthy discussion of the future of research in C. elegans, which I am sure will prove to be just as fruitful as its history.

Genetic screens are at the core of geneticist's arsenal of research tools due to their wide application and ability to be tailored to a specific experiment. They allow a researcher to narrow in on the process in question and begin to collect data, proving to be a very powerful and valuable technique. Based on the large variety of screen discussed in this review, I'm sure that a screen could be designed for any genetic experiment anyone wanted to do. Even you!

What Could Your Future Hold?

This month’s The Scientist hosted an article on Michael Hengartner. You might not have heard of him, but today he is a Dean at the University of Zurich and is held as one of the leaders in programmed cell death research. His journey to the top was one that he never expected. As an MIT graduate student who had a background in Biochemistry, Michael knew that he wanted to work with the protein NF-kappaB, a transcription factor that helps regulate a cell’s response to various stimuli. Even though he was determined to work with that protein, Hengartner attended a group meeting in another lab with his classmate. That meeting is where Michael met Robert Horvitz, who later mentioned to Hengartner that he was working a small side project investigating programmed cell death in C. elegans. Michael thought it was such a “stupid” concept that “an animal just threw away whole cells,” but the stupidity of it just made him determined to find out why first hand.

Ten years later Hengartner was still working with Horvitz’s lab researching programmed cell death, or apoptosis, pathways. The pathway that they discovered has three main stages: the killing of the cell, the engulfing of the cell by a neighboring cell, and then the digestion of the cell tissue by the neighboring cell. While in Horvitz’s lab Hengartner cloned and identified ced-9, a gene that prevents apoptosis from happening in certain cells of C. elegans. Mutants where then found that carried an overactive form of this gene, which caused cells that were supposed to die to actually live. He later found homology of this gene with a human gene called Bcl-2 which is known to be involved with some cancers.

Horvitz was using his apoptosis research to try to discover why some cancers occur, and the possibility of treatment. Horvitz stated, “We normally think of cancer as too much cell division, but cancerous growth really is a change in an equilibrium. If you have too much cell division, you get an increase in cell number; if you have too little cell death, you also get an increase in cell number. Either can lead to cancer.” Hengartner’s research in the Horvitz lab, especially the discovery of the homology between ced-9 and Bcl-2, which effectively linked underactive apoptosis as a possible cause of cancer, played a large role in Horvitz’s 2002 Nobel Prize in Physiology, and paved the way for a boom in apoptosis reasearch.

Although Hengartner was not given the Nobel Prize for all his efforts, his name was still known throughout the scientific community allowing him to get a lab of his own, and later move up the academic ladder to become a Dean. Inspired by his own fortune, Hengartner now tries to motivate the youth to find their true path. He invites high schoolers into the lab to help screen C. elegans for fluorescing dead cell markers, and has helped establish a new molecular life science PhD program. Overall, Michael is a role model for taking opportunities as they come and never looking back.

For More information here are some links to the magazine and Michael Hengartner's lab page:
http://www.the-scientist.com/
http://www.imls.uzh.ch/research/hengartner.html

The Cha Cha Cha theory of scientific discovery

How are great scientific discoveries made? A prominent scientist, Daniel Koshland, the discoverer of the induced-fit model for protein-ligand interactions wrote an article in Science a few years back describing three modes of scientific discovery:   "The Cha Cha Cha theory of Scientific discovery". The Cha's in title are short for charge, challenge and chance. Charge discoveries solve obvious problems for which the solution is not clear; Challenge discoveries  are made to account for an abundance of facts that don't quite fit together. The discoverer comes up with a model that can describe all of the anomolies. Finally Chance discoveries are those serendipitous discoveries that Louis Pasteur felt "favored the prepared mind. Check out the article and find your favorite scientific discovery on the chart. What controls the movement of sun earth and stars? why are there clear spots on my petri dish? Why do offspring look like their parents? Interesting quick read if you want to follow up a wonderful lecture by Professor Mel Green on his own scientific discoveries over the last half century.

http://www.sciencemag.org/cgi/content/full/317/5839/761