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SIRT1 and cancer

Sunday, October 26, 2008

In the past we've had some discussion of the histone deacetylase (HDAC) enzyme SIRT1 and other related sirtuin proteins, especially with respect to their possible relationship with longevity. (See here, for example.)

Much of the focus has been on the HDAC properties of SIRT1 that can switch off various genes. But there have also been findings of more direct relations between SIRT1 and cancer. Some indicate that sirtuins, including SIRT1, may help suppress cancer in certain circumstances, while others suggest it may actually help promote cancer. We'll have to save a general discussion of this relationship for later.

But now we have some research that shows how SIRT1 is directly involved, and has a beneficial effect, in an important pathway that's quite relevant to breast cancer.

The background is that the BRCA1 gene (short for breast-cancer-associated gene 1) is a tumor suppressor gene that, when mutated, may lose its ability to suppress tumors. Defective BRCA1 is sometimes inherited, which helps explain familial tendencies to breast cancer.

So what does BRCA1 normally do to suppress tumors? Well, apparently it maintains expression of SIRT1, which in turn inhibits the expression of another protein, called Survivin. The latter is an inhibitor of programmed cell death (apoptosis), and therefore, when it is active, helps protect cancer cells, which might otherwise be killed by the immune system, chemotherapy, or radiation.

In a nutshell: defective BRCA1 leads to insufficient SIRT1, which leads to an inadequate ability to kill cancer cells.

New Findings May Improve Treatment Of Inherited Breast Cancer (10/9//08)
About 8% of breast cancer cases are caused by mutations in tumor suppressor genes, such as breast cancer associated gene-1 (BRCA1). BRCA1 is the most frequently mutated tumor suppressor gene found in inherited breast cancers and BRCA1 mutation carriers have a 50-80% risk of developing breast cancer by age 70. "Although work with animal models of BRCA1 mutation has provided some insight into the many biological processes linked with BRCA1, very little is known about the downstream mediators of BRCA1 function in tumor suppression," says lead study author Dr. Chu-Xia Deng from the Genetics of Development and Diseases Branch at the National Institutes of Health.

Dr. Deng and colleagues were interested in investigating the relationship among BRCA1, SIRT1 and Survivin. SIRT1 is a protein and histone deacetylase involved in numerous critical cell processes including metabolism, DNA repair and programmed cell death, known as apoptosis. Although SIRT1 has been implicated in tumorigenesis, no concrete role in cancer initiation or progression has been identified. Survivin is an apoptosis inhibitor that is dramatically elevated in many types of tumors. Research has suggested that Survivin may serve to maintain the tumor and promote growth.

The researchers found that BRCA1 functioned as a tumor suppressor by maintaining SIRT1 expression, which in turn inhibited Survivin expression. When BRCA1 was not functioning properly, SIRT levels decreased and Survivin levels increased, allowing BRCA1-deficient cells to overcome apoptosis and undergo malignant transformation.

This leads one to ask whether there are other ways that SIRT1 activation could be maintained when BRCA1 is defective. Fans of resveratrol will observe that this is something that resveratrol can do. And so the researchers gave it a try:
They went on to show that the compound resveratrol strongly inhibited BRCA1-mutant tumor growth in cultured cells and animal models. ... In the current paper, resveratrol enhanced SIRT1 activity, this leading to reduced Survivin expression and subsequent apoptosis of BRCA1 deficient cancer cells.

Ironically, previous research had indicated circumstances in which SIRT1 might promote growth of other types of cancers. It might, for instance, inhibit expression of other tumor-suppressor genes.

Another news account goes into this a little more:

Gene thought to promote tumor growth has opposite role in a kind of breast cancer (10/9/08)
These results were surprising in light of previous reports showing that high levels of SIRT1 enhance growth of other types of tumors. It now appears that SIRT1 can enhance or inhibit tumor growth — it all depends on the context, says Deng. ...

The researchers also found that a red wine chemical called resveratrol, recently touted as a powerful antiaging compound, was effective in combating BRCA1-associated tumor formation specifically.

How resveratrol is able to do this is unclear. “The work in this case is that SIRT1 has an antitumor effect, and this paper provides mechanistic insights into that,” comments Pere Puigserver, a Harvard biologist who studies SIRT1. But the resveratrol data should be taken with caution, he notes. While this new research clearly shows the direct relationship between BRCA1 and SIRT1, the direct link between resveratrol and SIRT1 is more difficult to demonstrate.

Nonetheless, molecular details of BRCA1-related breast cancer are emerging, and this new data places SIRT1 squarely inside the complex web of molecules that impact tumor growth.

One of the main reasons that sirtuins are suspected of having cancer-promoting properties in some circumstances is that they may inhibit the highly important p53 tumor suppressor gene. (P53, when functioning properly, promotes cell apoptosis when DNA defects are detected during cell division.) In just one example of many, here's research from earlier this year that suggests a tumor-promoting property of sirtuins:

Switching on cancer killer gene (5/8/08)
Scottish scientists have discovered how to control a major anti-tumour gene that could lead to more effective chemotherapy. According to a report in the Cancer Cell Journal, research conducted by the Universities of St Andrews and Dundee may eventually lead to the development of new cancer drugs.

The gene, called p53 and known as "the guardian of the genome", is damaged or switched off in most cancers. But the resrchers found that they could reboot it using two new biological compounds called "tenovins".

In a laboratory study, the academics found that these compounds could kick-start p53 by turning off enzymes called sirtuins. Sirtuins act like genetic switches and keep p53 under control, ensuring that the cells stay alive.

Other news accounts of this research: here, here.

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Embryonic stem cell differentiaton

A typical mammal, like a human, has over 200 different cell types in its body, corresponding to tissue types such as liver, heart, brain, muscle, etc. Obviously, for each specialized type of cell to perform its function, rather different sets of genes have to be expressed. Yet the DNA of each cell type contains all the genes, whether they're needed or not. One may reasonably wonder what kind of mechanisms are used to keep unneeded (and unwanted) genes "out of the way" in fully differentiated cells.

Further, a multipotent stem cell, and especially a pluripotent stem cell, might be expected to manage its supply of genes somewhat differently than does a fully differentiated cell. If it does, the question of how is especially interesting with respect to "induced pluripotent stem cells" that are obtained by a relatively, and surprisingly, simple "reprogramming" of fully differentiated cells such as skin cells.

Some new research has begun to address these questions:

Unlocking Stem Cell, DNA Secrets To Speed Therapies (10/10/08)
In a groundbreaking study led by a molecular biologist at Florida State University, researchers have discovered that as embryonic stem cells turn into different cell types, there are dramatic corresponding changes to the order in which DNA is replicated and reorganized.

The findings bridge a critical knowledge gap for stem cell biologists, enabling them to better understand the enormously complex process by which DNA is repackaged during differentiation -- when embryonic stem cells, jacks of all cellular trades, lose their anything-goes attitude and become masters of specialized functions. ...

"Understanding how replication works during embryonic stem cell differentiation gives us a molecular handle on how information is packaged in different types of cells in manners characteristic to each cell type," said David M. Gilbert, the study's principal investigator. "That handle will help us reverse the process in order to engineer different types of cells for use in disease therapies."

"We know that all the information (DNA) required to take on the identity of any tissue type is present in every cell.... We must learn how cells lose pluripotency in the first place so we can do a better job of reversing the process without risks to patients.

"The challenge is, adult cells are highly specialized and over the course of their family history over many generations they've made decisions to be certain cell types rather than others," he said. "In doing so, they have tucked away the information they no longer need on how to become other cell types. Hence, all cells contain the same genetic information in their DNA, but during differentiation they package it with proteins into 'chromatin' in characteristic ways that define each cell type. The rules that determine how cells package DNA are complicated and have been difficult for scientists to decipher."

But, Gilbert noted, one time that the cell "shows its cards" is during DNA replication.

"During this process, which was the focus of our FSU research, it's not just the DNA that replicates," he said. "All the packaging must be replicated as well in each cell division cycle."

He explained that embryonic stem cells have many more, smaller "domains" of organization than differentiated cells, and it is during differentiation that they consolidate information.

"In fact, 'domain consolidation' is what we call the novel concept we discovered," he said.

The open access paper is available here:

Global Reorganization of Replication Domains During Embryonic Stem Cell Differentiation
Author Summary

Microscopy studies have suggested that chromosomal DNA is composed of multiple, megabase-sized segments, each replicated at different times during S-phase of the cell cycle. However, a molecular definition of these coordinately replicated sequences and the stability of the boundaries between them has not been established. We constructed genome-wide replication-timing maps in mouse embryonic stem cells, identifying multimegabase coordinately replicated chromosome segments—“replication domains”—separated by remarkably distinct temporal boundaries. These domain boundaries were shared between several unrelated embryonic stem cell lines, including somatic cells reprogrammed to pluripotency (so-called induced pluripotent stem cells). However, upon differentiation to neural precursor cells, domains encompassing approximately 20% of the genome changed their replication timing, temporally consolidating into fewer, larger replication domains that were conserved between different neural precursor cell lines. Domains that changed replication timing showed a unique sequence composition, a strongly biased directionality for changes in resident gene expression, and altered radial positioning within the three-dimensional space in the cell nucleus, suggesting that changes in replication timing are related to the reorganization of higher-order chromosome structure and function during differentiation. Moreover, the property of smaller discordantly replicating domains may define a novel characteristic of pluripotency.


Powerful Nearby Supernova Caught By Web

Monday, October 13, 2008

Powerful Nearby Supernova Caught By Web
This composite image shows the central regions of the nearby Circinus galaxy, located about 12 million light years away. Data from NASA's Chandra X-ray Observatory is shown in blue and data from the Hubble Space telescope is shown in yellow ("I-band"), red (hydrogen emission), cyan ("V-band") and light blue (oxygen emission). The bright, blue source near the lower right hand corner of the image is the supernova SN 1996cr, that has finally been identified over a decade after it exploded.

Optical images from the archives of the Anglo-Australian Telescope in Australia show that SN 1996cr exploded between February 28, 1995 and March 15, 1996. Among the five nearest supernovas of the last 25 years, SN 1996cr is the only one that was not seen shortly after the explosion. It may not have been noticed by astronomers at the time because it was only visible in the southern hemisphere, which is not as widely monitored as the northern.

Circinus galaxy with SN 1996cr – click for 576×480 image

Induced pluripotent stem cells IV

Sunday, October 5, 2008

Induced pluripotent stem cells (iPS cells) may again be judged one of the most significant scientific developments this year, and the news keeps coming. (Of course, it was near the top last year also.)

Some of our previous discussions are here, here, and here.

The ability to turn nearly any type of adult cell into the equivalent of a pluripotent stem cell seems almost too good to be true. And so far, that goal is still elusive, as a practical matter, with respect to treating diseases.

There have been at least three principal difficulties with experimental processes reported so far.

  1. The process depends on a kind of gene therapy that inserts a few desired additional genes into cellular DNA using certain types of viruses, and the process itself significantly raises the chances of affected cells becoming cancerous.
  2. One or more of the genes that are added to cellular DNA to induce pluripotency can also raise the chances of a cell becoming cancerous.
  3. Alternative methods that address the first two problems tend to be substantially less efficient, therefor slower and more expensive, for producing the desired iPS cells.

The research we'll consider here addresses the first of these problems.

Induced Pluripotent Stem Cells Generated Without Viral Integration
Pluripotent stem cells have been generated from mouse and human somatic cells by viral expression of the transcription factors Oct4, Sox2, Klf4, and c-Myc. A major limitation of this technology is the use of potentially harmful genome-integrating viruses. Here, we generate mouse induced pluripotent stem cells (iPS) from fibroblasts and liver cells by using nonintegrating adenoviruses transiently expressing Oct4, Sox2, Klf4, and c-Myc. These adenoviral iPS (adeno-iPS) cells show DNA demethylation characteristic of reprogrammed cells, express endogenous pluripotency genes, form teratomas, and contribute to multiple tissues, including the germ line, in chimeric mice. Our results provide strong evidence that insertional mutagenesis is not required for in vitro reprogramming. Adenoviral reprogramming may provide an improved method for generating and studying patient-specific stem cells and for comparing embryonic stem cells and iPS cells.

Perhaps a little more explanation would be in order. We've discussed the four transcription factors, Oct4, Sox2, Klf4, and c-Myc, in earlier articles.

The "insertional mutagenesis" mentioned here refers to the use of a type of virus that inserts some of its genes directly into the cellular DNA. Such viruses include lentiviruses and other retroviruses. HIV is an example of a lentivirus. The genetic material of this kind of virus is in the form of RNA, which must first be translated into DNA (by an enzyme called reverse transcriptase) and then integrated into the host cell DNA. The transcription factor genes are artificially added to the virus RNA so that they are copied along with everything else.

That integration step is what enables genes for the transcription factors to be inserted into host DNA. Although genes for those factors are already present, of course, in non-stem cells, they are in a form that is less readily translated into proteins than in pluripotent cells. The newly-integrated genes, however, can be easily translated, and they produce the protein transcription factors that go on to turn the cell into a pluripotent stem cell.

The drawback of this method is that the new genes can be inserted at arbitrary points of the host DNA, and this can harmfully affect other genes, which may make the cell susceptible to becoming cancerous.

What the research in this latest work has done is to add the transcription factor genes to a different kind of virus, called an adenovirus. The significant difference of an adenovirus from a retrovirus is that the genetic material of the former consists of double-stranded DNA, like the DNA of the host cell. When an adenovirus infects a cell, its DNA floats freely within the cell, and it can be translated into proteins by the same process as for the host cell DNA.

So what the new work described in this study does is to add the transcription factor genes to the adenovirus DNA, and then allow the virus to infect normal adult cells. This has the advantage of not damaging the host DNA, because it does not get integrated into it.

Naturally, this is an obvious approach to try, and it has been attempted before, but not successfully. The reason it hasn't worked before, probably, is that the adenovirus DNA is diluted every time an infected cell divides, since there may be, at most, only a couple dozen copies of the virus DNA in each infected cell. It does not get copied reliably into daughter cells, and that's a good thing on the whole. (Otherwise an infection might never go away.)

Fortunately, it turns out that simply having the adenovirus-carried transcription factor genes in a cell for a sufficiently long time can trigger further gene expression that confers pluripotency – which remains even after the virus genes are no longer present. Persistence pays.

The research was carried out using various types of mouse cells – fetal liver cells, adult hepatocytes, and fibroblasts from the mouse tail tip. The last of these can, of course, be obtained quite easily.

There is, however, a downside. The efficiency of inducing pluripotency by this method is still very low. Typically, only 0.0001% to 0.001% (1 in a million to 1 in 100,000) of cells are converted. This compares with 0.01% to 0.1% when DNA-integrating viruses are used.

The research proceeded to compare the adenovirus-induced pluripotent cells with natural pluripotent cells. The similarities were quite close:

  • Pluripotency genes of the reprogrammed cells lack methylation (a chemical modification that inhibits expression), just like the genes of natural pluripotent cells.
  • The pluripotency genes (including Oct4, Sox2, Klf4, c-Myc, and Nanog) of normal pluripotent cells are also expressed in the reprogrammed cells, even after all traces of adenovirus DNA are gone.
  • The iPS cells formed teratomas (cell masses consisting of many different cell types) when injected into adult mice.
  • When the iPS cells were injected into mouse blastocysts, which then developed into mostly normal, but "chimeric", young mice, evidence of descendants of the iPS cells turned up in many different tissue types.

The next step for research in this direction will be to find out whether the low efficiency of adenoviral reprogramming can be improved by techniques similar to those used to improve the efficiency of retroviral reprogramming.

News reports on this research:

M. Stadtfeld, M. Nagaya, J. Utikal, G. Weir, K. Hochedlinger (2008). Induced Pluripotent Stem Cells Generated Without Viral Integration Science DOI: 10.1126/science.1162494

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Hobgoblins, devils, and politics

Wednesday, October 1, 2008

The whole aim of practical politics is to keep the populace alarmed (and hence clamorous to be led to safety) by menacing it with an endless series of hobgoblins, all of them imaginary.
    -- H. L. Mencken

Political Attitudes Are Predicted By Physiological Traits, Research Finds (9/18/08)

Alford and his colleagues studied a group of 46 adult participants with strong political beliefs. Those individuals with "measurably lower physical sensitivities to sudden noises and threatening visual images were more likely to support foreign aid, liberal immigration policies, pacifism and gun control, whereas individuals displaying measurably higher physiological reactions to those same stimuli were more likely to favor defense spending, capital punishment, patriotism and the Iraq War," the authors wrote. ...

In a later session, they were attached to physiological measuring equipment and shown three threatening images (a very large spider on the face of a frightened person, a dazed individual with a bloody face and an open wound with maggots in it) interspersed among a sequence of 33 images. Similarly, participants also viewed three nonthreatening images (a bunny, a bowl of fruit and a happy child) placed within a series of other images. A second test used auditory stimuli to measure involuntary responses to a startling noise.

The researchers noted a correlation between those who reacted strongly to the stimuli and those who expressed support for "socially protective policies," which tend to be held by people "particularly concerned with protecting the interests of the participants' group, defined as the United States in mid-2007, from threats." These positions include support for military spending, warrantless searches, the death penalty, the Patriot Act, obedience, patriotism, the Iraq War, school prayer and Biblical truth, and opposition to pacifism, immigration, gun control, foreign aid, compromise, premarital sex, gay marriage, abortion rights and pornography.

It's this election season's well-timed release of a poli-psy research study connecting political behavior with behavior in general. And why shouldn't a particular type of individual behavior have something in common with other types?

Perhaps the main resistance to such a connection comes from the optimistic notion that ideological choices are somehow more "rational" and carefully thought out than other types of choices – like preferences for particular fragrances, colors, or ice cream flavors.

Or, at least, that political opinions are based on real-life experience rather than on whatever it is that shapes physiological responses.

We've been over similar ground a few times before. See here, here.

So what to make of this study? Political scientists generally accept that there are personality factors that correlate with political beliefs. Personality factors usually have both genetic and developmental roots. The genetic roots will also usually be expressed in various physiological attributes of an individual.

Just as genetic factors affect personality and behavior and physiology, it isn't unreasonable to suppose that personality and behavioral tendencies affect political beliefs. (Causation may well go in the other way, too, from beliefs to personality and behavior.) So it's not unreasonable that physiological attributes may also correlate with beliefs.

As far as this research is concerned – it's interesting, but quite a bit more data and research will be needed for a persuasive case.

Here's the actual abstract of the study:

Political Attitudes Vary with Physiological Traits
Although political views have been thought to arise largely from individuals' experiences, recent research suggests that they may have a biological basis. We present evidence that variations in political attitudes correlate with physiological traits. In a group of 46 adult participants with strong political beliefs, individuals with measurably lower physical sensitivities to sudden noises and threatening visual images were more likely to support foreign aid, liberal immigration policies, pacifism, and gun control, whereas individuals displaying measurably higher physiological reactions to those same stimuli were more likely to favor defense spending, capital punishment, patriotism, and the Iraq War. Thus, the degree to which individuals are physiologically responsive to threat appears to indicate the degree to which they advocate policies that protect the existing social structure from both external (outgroup) and internal (norm-violator) threats.

Unsurprisingly, given what time of the year it is, this research has received its share of media attention. For example:

Ideology in Your DNA? Not Quite (9/19/08)
The study had its limitations — the sample size was small and all of the subjects were white Nebraskans — but it’s still a small step toward a greater understanding our ever-increasing ideological divide, even if the answer doesn’t lie in our genes.

That political beliefs per se are not in our genes is obvious. What's in our DNA got there over the last 3 or 4 billion years, and the part that's specifically human, over the last 200,000 or so years. Contemporary ideologies were not around for most of that time. But what was around was a world that was usually hazardous to an organism's existence, so consequently a whole panoply of predispositions evolved to efficiently deal with threats. Of course, all individuals of a given species don't have exactly the same predispositions, because different strategies can be effective even in similar situations.

However, there is research that shows, based on twin studies, the probable existence of some genetic factors that correlate with political belief. For example:

Political Views May Be Genetically Influenced, Twin Study Shows (2/6/08)
Research by Rice University professor of political science John Alford indicates that what is on one's mind about politics may be influenced by how people are wired genetically.

Alford, who has researched this topic for a number of years, and his team analyzed data from political opinions of more than 12,000 twins in the United States and supplemented it with findings from twins in Australia. Alford found that identical twins were more likely to agree on political issues than were fraternal twins.

On the issue of property taxes, for example, an astounding four-fifths of identical twins shared the same opinion, while only two-thirds of fraternal twins agreed.

Not coincidentally, Alford is a co-author of the Science paper we're discussing. He also makes a good common-sense case for the role of genetics in understanding political opinion and behavior:
Alford believes that political scientists are too quick to dismiss genetics; rather, he believes genetics should be studied and taught along with social-environment influences.

"It has been proven that genetics plays a role in a myriad of different human interaction and makeup," said Alford. "Why should we exclude political beliefs and attitudes?"

Even more to the point, there are studies that show that the emotion of fear – fear of death, specifically – influences political opinion. In particular, the opinions that people express can be influenced by whether or not thoughts of death are on their minds. For example:

Fear of death may factor into who we vote for (12/21/05)
Authors of a study published in the latest issue of Analyses of Social Issues and Public Policy believe that voting behavior should be the result of rational choice based on an informed understanding of the issues. But using research based on the 2004 presidential election, they found that people may vote with their hearts, rather than their heads. Their findings demonstrated that registered voters in a psychologically benign state of mind preferred Senator Kerry to President Bush, but Bush was more popular than Kerry after voters received a subtle reminder of death.

(Another news report on this: here.)

Again, it shouldn't be all that surprising that having a fear of death in their minds could affect people's political opinions. After all, a fear of death certainly affects religious opinions. Death, speculation about an individual's fate after it occurs, and the fear of it, are central features of most religions. Religions generally compete among themselves to tell self-promotional stories about the favorable rewards that will accrue after death to true believers of the religion. And those religions which promise the most attractive rewards generally are the most successful.

Speculations about the evolutionary and social origins of religious belief generally assign an important role in those origins to human concerns and fears of death, and the way religious beliefs are constructed to help cope with those fears.

So if fear, and the ways that an individual typically deals with it, play a big role in religious opinion, why not in political opinion also? Of course, this would also explain well-known correlations between the religious and political beliefs of people. Religion and politics consist of ideologies with a lot of overlap.

As long as we're speculating, we may as well go all in and take note of important similarities between government and religion. In particular, government and religion are both social institutions created to deal with fears inherent in social living. Religion is primarily concerned with the fear of death itself, in any form, and secondarily with behavior of others or oneself that might threaten an individual's welfare. The latter concern is the province of "morality".

[Added 6/16/09: Here's Bertrand Russell's take on this: "Religion is based, I think, primarily and mainly upon fear. It is partly the terror of the unknown and partly, as I have said, the wish to feel that you have a kind of elder brother who will stand by you in all your troubles and disputes." - from Why I Am Not a Christian]

Government has these same two concerns, but generally in reverse order – except for extremes such as homicidal behavior and warfare. Government usually deals with less dire threats, but most political philosophers agree that one of its primary functions is to allay fears of the Hobbesian "war of all against all".

So government and religion are twin institutions that developed from the same seed – fear. Sometimes they are even Siamese twins, in theocracies and states with theocratic elements.

Let's go back now to the psychology of fear, and the question of how much role genetics may play in the experience of fear, physiological signs of fear, and hence a possible connection with political attitudes.

This is quite an interesting question in itself, and there is recent research that's relevant:

Mice Missing 'Fear' Gene Slow To Protect Offspring (9/15/08)
First, he discovered a gene that controls innate fear in animals. Now Rutgers geneticist Gleb Shumyatsky has shown that the same gene promotes "helicopter mom" behavior in mice. The gene, known as stathmin or oncoprotein 18, motivates female animals to protect newborn pups and interact cautiously with unknown peers.

This "fear gene" is highly concentrated in the amygdala, a key region of the brain that deals with fear and anxiety. Shumyatsky's newest finding could enhance our understanding of human anxiety, including partpartum depression and borderline personality disorders.

Here's a blog post on the research and here's the research abstract:

Stathmin reveals dissociable roles of the basolateral amygdala in parental and social behaviors
Innate parental behaviors and adult social interactions are essential for survival of the individual along with the species as a whole. Because these behaviors require threat assessment of the environment, it is plausible that they are regulated by the amygdala-associated neural circuitry of fear. However, the amygdala is not a single anatomic and functional unit, and nuclei of the amygdala have multiple inter- and intra-connections. This poses a question as to the exact role of different amygdala nuclei in these behaviors and the mechanisms involved. The basolateral complex of the amygdala nuclei (BLA) is particularly interesting in this regard: although the BLA role in forming memories for learned fear is established, the BLA role in innate behaviors is not well understood. We recently demonstrated that mice without an inhibitor of microtubules, stathmin, a gene enriched in BLA-associated circuitry, have deficiency in innate and learned fear. Here we show that the deficiency in fear processing in stathmin−/− females leads to improper threat assessment, which in turn affects innate parental care and adult social interactions.

Below are some blog commentaries on the political attitudes paper of Hibbing, Oxley, et al. It's interesting that these bloggers have expertise in biology, psychology, and neuroscience, but none seem to have a professional political science perspective (as some of the paper's co-authors do).

Some of these blog posts correctly point out methodological reasons why the study cannot be construed to "prove" a hypothesis. However, that does not seem to have been the intention of the researchers who did the study. I think they were more interested in finding plausible evidence for the hypothesis, as a first step to pursuing their ideas in more depth.

Additional news reports:

D. R. Oxley, K. B. Smith, J. R. Alford, M. V. Hibbing, J. L. Miller, M. Scalora, P. K. Hatemi, J. R. Hibbing (2008). Political Attitudes Vary with Physiological Traits Science, 321 (5896), 1667-1670 DOI: 10.1126/science.1157627

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