DRD4, Novelty Seeking, and Vervet Monkeys, Oh My!

Hey everyone,

Here is a link to a very cool article exploring the role of DRD4, a dopamine receptor gene, and novelty seeking behaviors in vervet monkeys. Dopamine receptors have been explored from multiple perspectives to determine their role in behaviors related to ADHD (e.g. hyperactivity, reinforcement and reward learning, novelty seeking, etc.)  This study measured whether either of the two DRD4 alleles in vervet monkeys was associated with an individual's willingness to approach a novel object placed into their living space. The shorter, five repeat variant of the DRD4 gene was found to be associated with novelty seeking. While the alleles found in vervet monkeys do not align with human variants, this research provides evidence that DRD4 is significant in novelty seeking behaviors and serves to further support the body of evidence implicating DRD4 in ADHD.

-Abi

Behavioral Genetics Potluck

THIS article deals with the idea that differences in levels of polymorphism of serotonin transporter and monoamine oxidase A genes can influence social structures between macaque species in a region.  Species of macaque with low agression and relaxed dominance structure (dominance structure is agression based) are functionally monomorphic at these loci.  More agressive and intolerant macaque species with strict hierarchy are polymorphic at these loci.

Nature Journal and Pot-Luck

Hey all,

Here's a piece in this week's Nature journal.  I think this already came up a few weeks ago, but yesterday I was reading about other animals in captivity and felt like sharing this about the chimps again.  The NIH is expected to retire several hundred of their chimpanzees, leaving just 50 or so available for research under the condition that their living environments are substantially improved. http://www.nature.com/news/time-called-on-chimp-work-1.12631

And for my pot-luck on behavioral genetics, here is a piece from the University of Texas at Dallas.  I'm not certain how valid it is, but behavioral genetics in terms of criminal behavior is pretty cool topic.  http://www.utdallas.edu/news/2012/1/24-15201_Criminologists-Research-Shows-Genes-Influence-Crim_article-wide.html

Genetic polymorphisms of serotonin and dopamine transporters in mental disorders

Hey guys, this is my potluck for this week (behavioral genetics).  My term paper for this class (and hopefully my research for this summer) is actually a topic of behavioral genetics regarding different polymorphisms in the serotonin transporter gene.  This study was done in humans, but my research will be with macaques.  Still, I thought this was an interesting study linking functional polymorphisms and monoamine transmission with diseases such as Parkinson’s and Huntington’s.

http://medical.med.tokushima-u.ac.jp/jmi/vol50/text/v50_n1-2_p025.html

Modular Descriptions of Behavior

One of the most interesting points to me in the Hoekstra papers was that current genomic research usually requires a quantifiable, discrete trait to analyze genetically, and that animal behavior seems to rarely exist in such modules.  However, This article lists many behaviors that are likely to act modularly and be controlled by a few genes, allowing for the possibility of genetic analysis on these behaviors.  The paper focuses mainly on mouse courtship and mating behaviors as well as the hormones and receptors known to influence them, demonstrating that apparently complex behaviors can sometimes be broken down into components which can be measured more quantitatively.  Finally, it discusses the potential neurological mechanisms of modular behaviors, such as genetic control of building neural pathways.  Though we are certainly a long way from understanding the genetics of very complex behaviors, these papers indicate that it really may be possible in cases of innate actions.

Personality Disorder, DSM-5, and Genetics

This article addresses some of the research issues encountered with behavioral genetics as it applies to human mental health. The DSM (Diagnostic and Statistical Manual of Mental Disorders) is a controversial but in many ways important tool for researchers seeking to improve treatment for mental illness spectrum disorders such as autism and schizophrenia. However, there is a lot of important dialogue in the field of behavioral genetics that discusses the extent to which the constructed (and inevitably distilled and in many cases socially problematic) definitions of certain "mental illnesses" encourage adherence to an inductive research paradigm where results are ultimately constrained by researchers' preconceived understandings of mental illness as formulated by the DSM. It is argued that this approach ultimately not only prevents better treatment but also often contributes to discrimination in healthcare. There are also clear cases, as with autism, of semantic oversimplification of what is a much more complex issue of genetic and environmental variation. I think these are important debates to think about when considering how behavioral genetics/genomics can be applied to human psychopharmacology.

http://ovidsp.tx.ovid.com/sp-3.8.1a/ovidweb.cgi?&S=FPIMFPDKOKDDNKDBNCOKFGGCPNNPAA00&Abstract=jb.search.27|1|1

Females Drive Primate Social Evolution

Given that we are focusing on behavioral genetics this week, I thought this article might be an interesting addition. It basically uses phylogenetic analysis to explore the extent to which females are drivers of social evolution in primates and concludes that they are the key sex to focus on when considering primate social behavior changes over time. There are also, however, some interesting theoretical assumptions about evolutionary and phylogenetic analysis that this paper's conclusion rests on that might be worth thinking about in tandem with some of the studies brought up this week. (For instance, what drives social evolution or what qualifies as behavioral genetic change might be understood very differently in varied research contexts.)

http://rspb.royalsocietypublishing.org/content/271/Suppl_3/S101.abstract?sid=b9820fad-6c6e-44c4-97b8-c7e9fe0fcbb1

On Why Talking about Behavioral Genetics is Important and Difficult

Genetic Differences and Human Identities
This article resulted from a 3 year study called "Crafting Tools for Public Conversation about Behavioral Genetics".  It explains to popular interest in the field of behavioral genetics, the possibilities as well as the limitations of research, and also many of the challenges and controversies surrounding the debate.  They raised thought-provoking questions like the implications of behavioral genetics on human freedom and human equality, as well as our conception of identity.  The paper merges the scientific and social ramifications of genetics and provides a very interesting and convincing explanation for why behavioral genetics is such an intense and controversial field.

These Weeks in Science

Hi all!  I am finally back to campus so I can once again journal stalk.  Somehow I missed three editions of Science, so here are the highlights.

March 8th

1) Perspective on (De)personalized Medicine.  This perspective article argues that without integrating social and environmental factors into a person's medical record, integrating genetic information will just lead to a new era of depersonalized medicine without really improving patient condition.

2) Report on Praire Dog Dispersal When All Close Kin Have Disappeared. This is an interesting article on behavioral ecology that illustrates the trade-off between kin competition and kin cooperation.

March 15th

1)News article on Bird Paleontology suggests that early birds may have had four wings instead of two. Not as related, but SUPER cool.

March 22nd

1)News article on Conservation Biology for amphibians.  This new center basically acts as life support for nearly extinct species.

Epigenetics Potluck

A study done by at doctor at the UNiversity of Massachusetts, shows that in humans, there small regions of the genome that are regulated in our neurons, that do not exist in other primates. Because the regulation is of human neurons, it is believed to account for much of our intellect and brain function. Aside from its function of increasing the ability of the human brain, it can also account for some diseases that occur only in humans such as Alzheimer's. The study focused on the specifics rather than the whole ( or as they called it the 'font' not the 'letters') of the DNA code which allowed them to observe if a gene was one that was present with a function or not in humans versus primates. The differences between whether the existing genomes were functioning or not, or their regulatory state, accounts for many difference between humans and primates and this this case, intellect. By mapping the epigenetics rather than sequencing genes, more discoveries can be made that are not as obvious because while genes may look the same, their function is what truly makes the difference.

http://www.eurekalert.org/pub_releases/2012-11/plos-teo111512.php

Genotype by Diet Interactions Effects on Cardiometabolic Responses

Significant Genotype by Diet (G × D) Interaction Effects on Cardiometabolic Responses to a Pedigree-Wide, Dietary Challenge in Vervet Monkeys (Chlorocebus aethiops sabaeus)
My potluck paper is from the January edition of the American Journal of Primatology on a study of vervet monkeys.  The study's goal was to confirm the interaction between nutrient composition of diet and genetic predispositions.  They also hoped to determine whether this applies to other cardiometabolic risk factors.  To test this, they changed the diet of a colony of vervet monkeys from the standard primate diet calorie allocation (18% protein, 13% fat, 69% carbohydrates) to a typical American diet calorie allocation (18% protein, 35% fat, 47% carbohydrates).  Most of the cardiometabolic phenotypes (except for weight) changed adversely.  Their results confirmed the interaction between nutrient composition of diet and genetic predispositions as well as the heritability of cardiometabolic phenotypes under dietary conditions.  Additionally, they found that these genetic effects varied in magnitude based on the diet.

420 Epigenetics Potluck 03/06

Here are some YouTube videos of a NOVA program on epigenetics.  Given the intended audience, the content is a bit basic given what we have already studied.  But they do raise a point of epigenetics and diseases.  NOVA discusses a pair of identical Spanish women: one has recently (at the time of the video) been diagnosed with cancer and the other is fearful that she will eventually be diagnosed, too.  They also discuss epigenetic therapy, trying to change the instructions of the cancer cells.  Both are interesting topics of discussion.

Part I -- https://www.youtube.com/watch?v=Xjq5eEslJhw
Part II -- https://www.youtube.com/watch?feature=endscreen&v=wFsxVkuChdU&NR=1

ANTH 420: Nature Journal

This week in Nature journal there were two pieces I want to share.

First is a news piece on using DNA testing to tackle illegal trade of elephant tusks.  We can use the information to trace back to the sites and elephant communities where poaching is most often happening in order to reinforce anti-poaching efforts.  This pertains to our primate studies because similar tactics have been implemented to control the sale of illegal primates as bush meat.  Meat can be tested to trace the poaching back to the source and also to squash the market for meat.  Here's the link for that bit: http://www.nature.com/news/tusk-tracking-will-tackle-illegal-trade-1.12510

Second, here are some circular RNA molecules that influence our gene expression by binding to and blocking microRNAs: http://www.nature.com/news/circular-rnas-throw-genetics-for-a-loop-1.12513

Role of Epigenetics in Aging Disorders

I found this article about the role of epigenetic changes in premature aging disorders.  Werner syndrome and Hutinson-Gilford Progeria are genetic disorders which had not been associated with a genetic cause until recently. Scientists in Spain studied the genetic profiles of WS and HGP patients and just discovered that DNA methylation patterns may have an impact on premature aging disorders.  DNA methylation patterns change with age, so certain methylation landscapes may be responsible for the phenotypic changes and susceptibility to certain diseases that accompany age-related processes. 

Epigenetics and Puberty

Current theories on the reaching of puberty involve the idea that adolescents need to reach a certain body weight or percent fat in order to trigger puberty, and the increasing weights of children can explain why the average age of puberty is decreasing.  This article introduces an epigenetic mechanism in which the expression of a gene Kiss1 is regulated by levels of PcG proteins which are in turn regulated by epigenetic mechanisms.  By interfering with this process, researchers were able to delay puberty in mice.  However, it might be some time before we can get excited over understanding the mechanism in humans or even non-human primate puberty regulation.

On the Topic of Catchy Science Headlines...

A new paper coming from Brown, advertised as "Does the villainous 'selfish gene' undermine genome's police?" was released today.  The article turns out to describe an interesting process by which a segregation disorder-gene (SD) seems to destroy sperm that contain a different allele.  The allele that triggers the reaction is called Responder, which replicates in its segment of DNA, acting as a parasite to the genome.  SD provides cytoplasm with enzymes that target Responder such that when the cells divide in meiosis, Responder-laden sperm are destroyed.  This mechanism seems pretty amazing to me, but perhaps not in the way implied by its headline...

Epigenetics Potluck

So this potlock is a couple of steps away from pure epi, but the theory does rest upon epigenetic markers and is probably one of my favorite theories--(do those exist?)
THIS is Badcock and Crespi's theory of the role parental conflict in fetal development and its role in susceptibility for autism-psychosis spectrum disorders (as well as Angelman's vs Prader-Willi).  The epigenetic part of this is that the chromosome is epigenetically marked for different expression in the father and the mother.  Therefore, CNV of the same gene can have different results based upon whether this variation is on the maternally inherited or paternally inherited chromosome.  Badcock and Crespi showed that this mechanism might account for some of the differences in susceptibility for autism or psychosis spectrum disorders.  When a paternally inherited gene is more expressed, the fetus is more likely to develop autism.  If the maternally inherited gene is more expressed, the fetus is more likely to have psychosis.

Evolving approaches to the ethical management of genomic data

Continuing our discussion on the ethics of obtaining genomic data, I am posting this review from Trends in Genetics.  Even when an individual’s name is stripped of his genomic data, there are still many ways to re-identify this individual.  Obtaining the permission of an individual to use his DNA doesn’t cut it for ethical protocol.  Plummeting costs to sequence entire genomes and the wide availability of genomic data makes this issue much more challenging. 

http://ac.els-cdn.com/S0168952513000267/1-s2.0-S0168952513000267-main.pdf?_tid=ba847f9e-85e3-11e2-b67d-00000aab0f01&acdnat=1362522570_74410ba39a94c9775344ad009f1ae21f

Increased methylation variation in epigenetic domains across cancer types.

Interesting publication quantifying epigenetic effects on tumor heterogeneity, which is one factor that makes cancer diagnosis quite difficult.  The authors of this paper looked specifically at DNA methylated regions in colon cancer cells of normal individuals vs diseased individuals.  They showed that cancer caused loss of epigenetic stability, which contributed to tumor heterogeneity.

http://www.ncbi.nlm.nih.gov/pubmed/21706001