I’m very glad to finally initiate Abstract 2.0. I hope this resource will be of great help to anyone willing to utilize it.
For now, I have set up a separate website for the submission and archiving of abstracts by those who contribute. The website is http://abstracts.sciofrelief.com.
Here is an example of a re-written abstract:
Colleen T. O’Loughlin, Laura C. Miller, Albert Siryaporn, Knut Drescher, Martin F. Semmelhack, and Bonnie L. Bassler (2013) 110:17981–17986, doi:10.1073/pnas.1316981110
A quorum-sensing inhibitor blocks Pseudomonas aeruginosa virulence and biofilm formation
Quorum sensing is a way a bacterium communicates to the cells around it to regulate behavior of the community as a whole. This process occurs in harmless bacteria as well as pathogens. One such pathogen, Pseudomonas aeruginosa, uses quorum sensing to attack its host in a concerted effort by all the cells present and to control how the cells ‘stick’ together once infecting the host. In an effort to prevent P. aeruginosa attack and infection, researchers tested synthetic molecules to identify those which block cells from receiving the attack message. One such molecule, meta-bromo-thiolactone (mBTL), succeeded in blocking the message and protected a roundworm model system and human lung cells from dying due to infection. The paper also discusses how mBTL works at the molecular level. The results from this study could help control complications in cystic fibrosis and hospital infections due to contaminated equipment.
I have sat on this long enough. It’s not like a have anything else going on right now (except the birth of a son in a month, syllabus to write, classes to prepare, evaluations to do, data to journal, …). Introducing:
Here are the details presently. I and anyone willing to help will scour the journals of our respective fields and choose those we feel need to be disseminated to the larger public. In a short synopsis (abstract if you will), an overview of the article and why it is important will be written and deposited here. Details will be worked out on how to submit the abstracts in the near future.
Now is the time to act (or later if now is not convenient)!
The science gap is huge. One of the biggest misconceptions hindering the advancement of scientific literacy in society is also one of the most crucial – the scientific method. And no wonder. Most people would look back at primary and secondary school and cringe when thinking about all the facts and concepts they had to memorize in science classes. I cringe when I think of the public concluding science is static and just the sum of all data gathered through the centuries.
The scientific method is dynamic and so is the collection of accepted scientific knowledge
Nothing in science is certain. In the words of the great Richard Feynman:
We absolutely must leave room for doubt or there is no progress and no learning. There is no learning without having to pose a question. And a question requires doubt. People search for certainty. But there is no certainty. People are terrified — how can you live and not know? It is not odd at all. You only think you know, as a matter of fact. And most of your actions are based on incomplete knowledge…
The idea that scientific knowledge is like a statue is a horrible, infectious disease in society. Consider this…
The scientific method is a bucket. This is not just any bucket; it holds all the scientific knowledge gathered throughout history. The bucket is just a utilitarian tool for collecting knowledge. Luckily, this bucket has a hole in the bottom. The scientific method is a two way street and is objective just like a bucket is just a bucket. At the beginning of it all, the bucket was filled with crystal clear water. Mother Nature had filled it for us but all its contents were a complete unknown. As human inquiry began, discoveries were like drops of color that allowed us to have a glimpse of the contents as it dispersed like food coloring in a glass of water. Each new discovery or observation adds a touch of color to the bucket. Nature’s true color will not be observed in our lifetime or possibly at all. Our curiosity and practice only adds to the hue within the bucket.
Sometimes we don’t know the hue of the water is wrong until new knowledge is obtained and added to the large bucket. With addition of the new color, drops of discolored water pour from the hole in the bucket. Soon the prevailing knowledge is uniform within the bucket. Science never sleeps so this constant increase in knowledge and data get us one step closer to the true color of the universe, or so we think until we find out the hue is all wrong as the hole opens and a novel color drops in.
Thank you, Congress, for your objective and far-sighted vision showing the nation is your top priority and you are looking out for its best interest. The most recent survey data from the National Science Foundation shows the general public overwhelmingly supports federal funding of basic research:
Since 1985, NSF surveys have asked Americans whether, “even if it brings no immediate benefits, scientific research that advances the frontiers of knowledge is necessary and should be supported by the federal government.” In 2010, 82% agreed or strongly agreed with this statement; 14% disagreed.
Not only does the public support federal funding for science and engineering research, they also hold high esteem for scientists, second only to firefighters and ahead of doctors, teachers, and members of the clergy. In another section, 91% of surveyed Americans are at least moderately interested in scientific discoveries. So, there is hope Americans can become more science literate.
Sequestration takes toll on research, education (universityofcalifornia.edu)
Welcome to part 4 of how bacteria make decisions. Parts 1 and 2 dealt with chemotaxis. Part 3 was a look at two component signaling systems. This part will deal with my favorite aspect of bacterial decisions for several reasons. Second messengers are common from bacteria to humans. The major second messenger we all learn about in biochemistry class is cyclic AMP (cAMP). However, bacteria use several nucleotides as second messengers. Many are used as determinants in the decision making process, but one of the most recently discovered (and personal favorite) is cyclic-di-GMP, or c-di-GMP.
Bacteria are constantly processing signals both inside and outside their cell membranes. Hard to believe that one of the most abundant response molecules was only discovered in the late 1980s while researching how a certain species, Acetobacter xylinumnow known as Gluconacetobacter xylinus, produced cellulose. Almost by accident, the Benziman lab discovered the enzyme responsible for cellulose production (cellulose synthase) was regulated by a nucleotide, later found to be c-di-GMP. Since that discovery, c-di-GMP has become a hot topic among microbiologists and immunologists due to the decisions bacteria make as the level of c-di-GMP increases within the cell. As I learned it, the concentration of c-di-GMP had predictable outcomes on the decisions of bacteria: high levels leads to loss of motility, increase in biofilm formation, changes in cell morphology, and increase in cell-cell communication. When low levels of c-di-GMP are present, the cell decides to move around (motility), become resistant to heavy metals, and, most importantly, becomes virulent. For example, Vibrio cholerae, the bad guy responsible for cholera, only decides to move around and produce cholera toxin when c-di-GMP levels are low in the cell. If levels increase, V. cholerae will produce biofilms via extracellular polysaccharide (EPS) production.
You might be asking yourself what controls the c-di-GMP levels of a bacterial cell. The initial discovery in the Benziman lab also found the enzymes/proteins that were responsible for making and breaking the second messenger. The long (and short) names are; for making c-di-GMP from 2 GTP molecules, diguanylate cyclases (DGCs aka GGDEF proteins) and degradation by phosphodiesterases (PDEs aka EAL proteins). GGDEF and EAL proteins are so called due to important amino acids necessary for their functions, GGDEF is glycine, glycine, aspartate, glutamate, phenylalanine, and EAL is glutamate, alanine, leucine. These enzymatic activities are usually controlled by regulatory protein domains common in bacteria (and humans). Signals from the environment (internal or external) can trigger changes in enzyme activity of GGDEFs and EALs thus changing the cellular concentration of c-di-GMP. This mechanism is well understood after 30 years of research. However, what happens next is still essentially unknown.
Cyclic-di-GMP levels rise within a bacterial cell. Now what? It was known early on that c-di-GMP itself could then interact with GGDEFs to inhibit activity. But what other proteins interact with c-di-GMP and help these bacteria decide to make major lifestyle changes? It wasn’t until 2006 that bioinformaticians predicted c-di-GMP binding to a protein, or protein domain. PilZ, an obscure protein of unknown function but necessary for Type IV pili motility, was hypothesized to bind c-di-GMP. By the end of 2007, this prediction was verified and PilZ domain proteins were the first shown linking c-di-GMP to downstream proteins in pathways, or circus rings.
Transitioning from a free swimming/moving cell to life in a biofilm community is a major lifestyle change for bacteria. This decision takes commitment which is initiated by a small molecule. In the next installment, we will get to the heart of current research.
I’m not a scientist at the bench anymore. My wife told me I had to stop playing and get a real job (a.k.a. graduate). However, I have very fond memories of my days studying chemotaxis. I will discuss that tomorrow in the second installment of My Tiny Highlight (MyTH) series. Bacteria, despite all modes of intimidation, do not follow our commands. They dance to the beat of a different drum, internal programming. Following the scientific method is easy but hard. You can make observations all you want (in my case 6 and half years and over 40 hours of video), but describing why things with the cell are happening or how they happen is a process. Finding explanations for what you observe and designing experiments to test them teaches humility because inevitably the cells will prove you wrong.
There is not much bravado in science. Failure is much more common than success and I would not have it any other way. I learned ten times more from failure than success. My dissertation project was split into two main goals dealing with two different proteins within a single bacterium, let’s call them protein1 (due to embargo and not published yet) and Tlp1 (since one paper is already published). It took 4 years of mostly failure with P1 to open my eyes and look outside the box. Breakthrough! Tlp1 was more straight forward, at least I thought at first. I still failed to explain my observations for a few years. Once I started visualizing the inside of the cell, with all its organized chaos, I started to be more creative in my hypotheses. Ultimately, we discovered a sort of paradox to everything found in the literature about the bacterial second messenger cyclic-di-GMP (c-di-GMP). I can’t wait for it to be published.
Grad school taught me a lot. I learned that if you love what you do, it doesn’t seem like work. Most of all, I learned that failure is a good thing because it takes us outside the box which is usually where the correct answers are.