11 Science Journalist Fellows at MIT

Posted on May 30, 2008 No Comments

The Knight Fellowship at MIT has a class of eleven science journalists from six countries this year. All are mid-career journalists who work for general interest news media to improve the public understanding of science. They will take a sabbatical year from their jobs to improve their knowledge by taking courses at MIT and Harvard, interviewing scientists and attending various seminars and lectures during the 2008–2009 academic year. They take up residence in Cambridge in August 2008.

The fellows include: Kimani Chege, editor of TechNews Africa, from Kenya; Sabin Russell, medical writer at The San Francisco Chronicle, from the USA; Teresa Firmino, science and technology reporter for Público, from Portugal; Jonathan Fildes, science and technology reporter for BBC News, from England; and Rachel Zimmerman, health and medicine reporter for The Wall Street Journal, from the USA.

This is a great program to help some excellent science journalist to get even better. We need more excellent science journalism.

We list the Knight Science Journalism Tracker on the list of our favorite science and engineering blogs.

Related: Science JournalismScience and Engineering Fellowship DirectoryReport on the Use of Online Science Resources

E. Coli Individuality

Posted on April 22, 2008 2 Comments

Expressing Our Individuality, the Way E. Coli Do by Carl Zimmer

A good counterexample is E. coli, a species of bacteria that lives harmlessly in every person’s gut by the billions. A typical E. coli contains about 4,000 genes (we have about 20,000). Feeding on sugar, the microbe grows till it is ready to split in two. It makes two copies of its genome, almost always managing to produce perfect copies of the original. The single microbe splits in two, and each new E. coli receives one of the identical genomes. These two bacteria are, in other words, clones.

A colony of genetically identical E. coli is, in fact, a mob of individuals. Under identical conditions, they will behave in different ways. They have fingerprints of their own.

E. coli appears to follow a universal rule. Other microbes exploit noise, as do flies, worms and humans. Some of the light-sensitive cells in our eyes are tuned to green light, and others to red. The choice is a matter of chance. One protein may randomly switch on the green gene or the red gene, but not both.

In our noses, nerve cells can choose among hundreds of different kinds of odor receptors. Each cell picks only one, and evidence suggests that the choice is controlled by the unpredictable bursts of proteins within each neuron. It’s far more economical to let noise make the decision than to make proteins that can control hundreds of individual odor receptor genes.

Identical genes can also behave differently in our cells because some of our DNA is capped by carbon and hydrogen atoms called methyl groups. Methyl groups can control whether genes make proteins or remain silent. In humans (as well as in other organisms like E. coli), methyl groups sometimes fall off of DNA or become attached to new spots. Pure chance may be responsible for changing some methyl groups; nutrients and toxins may change others.

Related: AndrogenesisSick spinach: Meet the killer E coliParasite Rex

Amazing Designs of Life

Posted on April 19, 2008 1 Comment

The More We Know About Genes, the Less We Understand by Carl Zimmer

All living things, ourselves included, turn genes on and off in a similar way, by making switch-like proteins called transcription factors. And as scientists have identified more of these, they’ve discovered something remarkable: They form a chain of command. The job of some transcription factors is to switch others on and off, and they in turn are controlled by other transcription factors. Even a seemingly simple microbe like E. coli has an impressive hierarchy. Just nine genes rule over about half of the 4,000-odd genes in E. coli.

E. coli’s network allows it to respond quickly to the challenges it meets, from starvation to heat to the loss of oxygen. It can rapidly reorganize itself, switching on hundreds of genes and switching off hundreds of others. What makes this network all the more impressive are the feedback loops that keep it from spinning out of control. When one gene switches on, for example, it may make a protein that shuts down the gene that switched it on in the first place.

Yet even as scientists uncover this network, they discover yet another mystery. In the latest issue of Nature, scientists reported an experiment in which they wreaked havoc with E. coli’s network. They randomly added new links between the transcription factors at the top of the microbe’s hierarchy. Now a transcription factor could turn on another one that it never had before. The scientists randomly rewired the network in 598 different ways and then stepped back to see what happened to the bacteria.

You might expect that they all died. After all, if you were to pop open the back of an iPod and start linking its components together in random ways, you’d expect it to crash. But that’s not what happened.

About 95 percent of the rewired bacteria did just fine with their new networks. They went on with their lives, feeding, growing and dividing. Some even performed better than microbes with the original wiring, under some conditions.

Related: Programing BacteriaSick spinach: Meet the killer E coliBacteria Can Transfer Genes to Other BacteriaEvolution is Fundamental to Sciencegenes tagged posts


Posted on April 1, 2008 No Comments

All Dad by Carl Zimmer

This week’s revelation is androgenesis. Androgenesis is what happens when kids get all their genes from their father.

Androgenesis, it turns out, transforms fatherhood into a parasitic invasion. It begins like normal fertilization, with a sperm fusing to an egg. But then the egg’s DNA gets hurled out of its nucleus, so that the sperm’s genes are the only ones left in the egg. The egg begins to develop into an embryo, but only after it has lost the mother’s DNA.

Related: Bdelloid Rotifers Abandoned Sex 100 Million Years AgoOne Species’ Genome Discovered Inside Another’sSex and the SeahorseFemale Sharks Can Reproduce AloneExplaining Genetics

Scientists Search for Clues To Bee Mystery

Posted on February 24, 2008 5 Comments

Honey Bees Give Clues on Virus Spread by Carl Zimmer

Now, as farmers wait anxiously to see if the honeybees will suffer again this spring, the true cause of CCD remains murky. Skeptics have raised many reasons to doubt that Australian viruses are to blame. In Australia, bees that get Israeli acute paralytic virus don’t get sick, and the country has had no reports of CCD. And in places where honeybee colonies are collapsing — Greece, Poland, Spain — there are no imported Australian bees. These are not the sort of patterns you’d expect, the skeptics say, if Australian viruses were killing American bees.

Whether scientists look inside a honeybee or look at the entire biosphere, nature is proving to be awesomely intricate. In the oceans and the soil, metagenomics is revealing millions of different kinds of microbes, with an almost inconceivable diversity of viruses shuttling between them, carrying genes from host to host. But we have almost no idea how these menageries work together, either in the biosphere or inside a host like a honeybee — or a human. Many of the microbes that metagenomics is revealing are entirely new to science. As genetic databases fill with DNA sequences from millions of new species, our scientific wisdom lags far behind.

How true. Watching as scientists try to work out what is going on with Colony Collapse Disorder is a great lesson in how scientists search for answers. As I stated earlier much of science is not about simple obvious truths but a search through confusing signs to try and determine what is going on. Answering why, is not always so easy as it appears when someone has already found the answer and posted it online.

Related: Virus Found to be One Likely Factor in Bee Colony Collapse DisorderBee Colony Collapse DisorderMore on Disappearing Honeybeesmost Carl Zimmer related posts

Parasite Rex

Posted on January 17, 2008 7 Comments

Parasite Rex is a great book by Carl Zimmer (one of the bloggers listed in the Curious Cat directory of science blogs). This is the first book read as part of my specific plan to read more about bacteria, cells, virus, genes and the like.

One of the most enjoyable aspects of writing this blog is that I have focused much more on cool things I read. And over time the amazing things I posted about related to these topics made me realize I should put some focused effort to reading more on these topics. Some of the posts that sparked that idea: Tracking the Ecosystem Within UsInner Life of a Cell: Full VersionWhere Bacteria Get Their Genes, People Have More Bacterial Cells than Human Cells, Biological Molecular MotorsEnergy Efficiency of DigestionOld Viruses Resurrected Through DNAMidichloria mitochondriiMicrobesUsing Bacteria to Carry Nanoparticles Into CellsHow Bacteria Nearly Destroyed All LifeNew Understanding of Human DNASoil Could Shed Light on Antibiotic ResistanceSymbiotic relationship between ants and bacteria

Parasite Rex was a great place to start. Carl Zimmer is a great writer, and the details on how many parasites there are and how interconnected those parasites are to living systems and how that has affected, and is affecting, us is amazing. And the next book I am reading is also fantastic: Good Germs, Bad Germs. Here is one small example from Parasite Rex, page 196-7:

A person who dies of sickle cell anemia is less likely to pass on the defective gene, and that means the disease should be exceedingly rare. But it’s not – one in four hundred American blacks has sickle sell anemia, and one in ten carries a single copy of the defective gene. The only reason the gene stays in such high circulation is that is also happens to be a defense against malaria.

Malaria is a parasite. One of the amazing things with repeated examples in the book were parasites that seemed to have extremely complicated life cycles (that don’t seem like a great strategy to prosper but obviously work). Where they grow in one life form (an insect or mammal or whatever) but must leave that life form for some other specific life form for the next stage in life (they cannot have descendants without doing so…). Seems like a crazy way to evolve but it happens over and over again.
Read more


Posted on June 8, 2007 1 Comment

New Life, New Patent by Carl Zimmer:

ETC is right in suggesting Venter might become “Microbesoft”–controlling operating system for anyone who wants to build an organism from scratch. Other researchers, such as Keasling, are promoting a different way of doing synthetic biology–what they call open source biology. Scientists and their students are amassing an open inventory of parts that anyone can use to design organisms of their own. And it’s open source biology, these researchers argue, that will provide the best protection against any evil uses of synthetic biology. Instead of being hidden behind patents, the information about these parts would be available to everyone, and collectively solutions could be found. As this debate starts to unfold, I think open source biology will keep it from becoming nothing but deja vu.

I support keeping science open. Patents are a tax on society that the government grants inventors for their efforts, in order to benefit society, by encouraging the inventors to innovate. The end is benefiting society. The means is granting a right of the patent holder (a right they do not have without patent law) that will encourage them to make the effort to innovate. I support the proper use of patents, but we have perverted the patent process into something that harms society. The system needs to be fixed. And the whole area of patents on life I find very questionable.

Related: Open-Source BiotechThe Effects of Patenting on Science by the AAASSoftware Patents – Bad IdeaInnovation Impact of Companies and Countries

Open Access and PLoS

Posted on May 28, 2007 2 Comments

In An Open Mouse, Carl Zimmer discusses the conflict between closed journals and those that support open access.

And what do I now hear from PLOS? Do I hear the grinding of lawyerly knives? No. I hear the blissful silence of Open Access, a slowly-spreading trend in the journal world. PLOS makes it very clear on their web site that “everything we publish is freely available online throughout the world, for you to read, download, copy, distribute, and use (with attribution) any way you wish.” No muss, no fuss. If I want to blog about this paper right now, I can grab a relevant image right now from it.

His post mentions the recent bad publicity Wiley received. It seems to me the Journals still don’t understand that their copyright of research results paid for by public funds are not going to continue. And that open access science is clearly the way of the future that their continued failure to deal with is increasing the odds monthly that they will find themselves on the outside of those practicing science in the 21st Century.

PLoS on the other hand recently hired Bora Zivkovic as PLoS ONE Online Community Manager. He will be great and continue to build PLoS into an organization supporting free and open science. I loved PLoS proactive action recounted by Bora, he posted that he was interested in the job:

Next morning, I woke up to a comment by the Managing Editor of PLoS ONE asking if my blog-post should be considered as a formal job application. My comment in response was a Yes.

Related: The Future of Scholarly PublicationAnger at Anti-Open Access PR

Virus Traps

Posted on March 27, 2007 No Comments

Scientists Explore Ways to Lure Viruses to Their Death by Carl Zimmer:

Viruses invade a cell by latching onto certain proteins on its surface. Once attached, they can slip inside the cell and manipulate it into making new copies of themselves. But viruses cannot infect red blood cells. Unlike most other cells in the body, as red blood cells develop in bone marrow they lose their DNA. If a virus ends up inside a red blood cell, there are no genes it can hijack to replicate itself.

“It occurred to us that if a virus bound to a red blood cell, that was a dead end,” said Dr. Robert W. Finberg, a professor at the University of Massachusetts Medical School.

To test the model, the scientists mixed normal bacteria with different levels of mutant traps and then infected them with viruses. After letting the viruses replicate, the scientists took a small sample to start a new colony. They discovered there was indeed a trap threshold above which the virus population could not survive. Above that threshold, the viruses disappeared by the time the scientists started the third round of colonies.

Related: Old Viruses Resurrected Through DNAVirus population extinction via ecological traps

Learning About the Human Genome

Posted on March 19, 2007 1 Comment

You Don’t Miss Those 8,000 Genes, Do You? by Carl Zimmer:

Science moves forward by flow. One experiment leads to another. Observations accrue. What seem like side trips or even dead ends may bring a fuzzy picture further into focus. Yet science often seems as if it moves forward one bombshell at a time, marked by scientific papers and press conferences.

When Craig Venter and his colleagues published their rough draft of the human genome in 2001 they identified 26,588 human genes. They then broke those genes down by their functions. Some were involved in building DNA, some in relaying signals, and so on. Remarkably, though, they classified 12809 genes–almost half–as “molecular function unknown.” Last week I wanted to know if those numbers still hold.

They weren’t so easy to find. In 2003 some reports came out to the effect that the genome had shrunk down to 21,000 genes. But I couldn’t turn up much news in the past four years.

The pie shows that we’re now down to just 18,308 genes. That’s over 8,000 genes fewer than six years ago. Many sequences that once looked like full-fledged genes, capable of generating a protein, now don’t make the grade. Some genes turned out to be pseudogenes–vestiges of genes that once worked but have been since wrecked by mutations. In other cases, DNA segments that appeared to be parts of separate genes have turned out to be part of the same gene.

Today scientists still don’t know the function of 5898 genes in the human genome. In other words, over the past six years about 7,000 genes either have been figured out or have vanished into the land of nevermind.

Great post. Read it.

Communication Emergence in Robots

Posted on February 24, 2007 No Comments

Evolving Robotspeak by Carl Zimmer:

At first the robots just flashed their lights at random. But over time things changed. In the trials with relatives undergoing colony selection, twelve out of the twenty lines began to turn on the blue light when they reached the food. The light attracted the other robots, bringing them quickly to the food. The other eight lines evolved the opposite strategy. They turned blue when they hit the poison, and the other robots responded to the light by heading away.

Two separate communication systems had evolved, each benefiting the entire colony. By communicating, the robots also raised their score by 14%. Here’s a movie showing six of these chit-chatting robots finding a meal.

Related: The original paper, Evolutionary Conditions for the Emergence of Communication in Robots (pdf) by Dario Floreano, Sara Mitri, Stephane Magnenat and Laurent Keller – more robot related posts