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- Doug on Will the Long History of Breast Cancer Research Culminate with Epigenetics Based Personalized Medicine?
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Finally there’s research comparing the epigenetic marks of human brain neurons to those of other primates, and it’s found real differences that make us function in a unique way. Do these epigenetic modifications help give us the brainpower for reflection, sentience, sapience, consciousness, and so forth? I’m not a gambler, but since primate neuron-specific genes don’t show a whole lot of difference from one another in their protein-coding sequences, that’s where I’d put my money. If I really had to.
With only one study to look at so far, this line of inquiry is in its infancy, to be sure. No one else has looked at the epigenetic component of human brain evolution. Hennady Shulha, Jessica Crisci, and Schahram Akbarian at the University of Massachusetts Medical School — and colleagues — took that first step with research they published in PLoS Biology late last month.
[Update 12/20/2012: Twitter friend @ed vautier points me to this study in Epigenetics, which documents the evolution of additional CpGs in humans, compared to non-human primates, and looks at their relative methylation levels. It's not neuron-specific, but it's in the same bucket as this study, so I thought I'd note it here. And so I have. And there you have it.]
What they find is this: Human prefrontal cortex neurons sport 33 epigenetic modifications — histone H3 trimethylated at lysine 4, or H3K4me3 — in genomic locations where macaques and chimps are much less likely to feature them. These H3K4me3 marks tended to appear near each other, and when the research team used chromosome conformation capture to look more closely at the region around one gene, DPP10, they discovered that chromosome looping appears to allow two nearby H3K4me3 modifications to come into contact.
But although H3K4me3 marks often lead to higher gene expression levels, this interaction seems to cause down-regulation of DPP10 through an interesting mechanism. As it turns out, increased anti-sense DPP10 RNA might be the answer. When the team did RNA-seq and quantitative RT-PCR on cortex neuron samples from separate human subjects, they found high levels of DPP10‘s anti-sense RNA and lower levels of DPP10 sense mRNA, as compared to the analogous macaque and chimp neurons.
The team also found the anti-sense RNA at higher levels in the human subjects’ neuron-rich prefrontal cortex layers II-IV, but not in neuron-poor layer I, white matter, or cerebellar cortex.
What’s more, the researchers discovered that the sequence of anti-sense DPP10 RNA has GC-rich areas that could allow it to form a stem-loop structure to interact with Polycomb 2 and transcription start sites — qualities that would support the RNA’s role in regulation.
Now, there’s no disease known to result from any DPP10 epigenetic modifications. But the authors note that rare variants “confer strong genetic susceptibility to autism, while some of the gene’s more common variants contribute to a significant risk for bipolar disorder, schizophrenia, and asthma.” That is, it’s a pretty good candidate for a gene that affects cortex function: Also according to the authors, it encodes a dipeptidyl peptidase-related protein that regulates potassium channels and neuronal excitability.
(It goes beyond DPP10, too. Five other genes associated with some of the 33 human-specific H3K4me3 peaks have ties to psychiatric diseases.)
So does all this point to an epigenetic role in human brain evolution? It starts to look even more convincing, considering what the researchers report about genetic changes in the DNA around these H3K4me3 marks, since the DNA sequence might very well have an important influence on histone binding and other functions. Compared to macaques, chimps, gorillas, and orangutans, the human versions of these DNA sequences have undergone major changes, with nucleotide substitution rates of 2- to 5-fold.
Meanwhile, nearby protein-coding sequences remained relatively unchanged in humans, as compared with the other primates. Also, compared to our close hominid relatives Homo denisova and Neanderthals, the nucleotide substitution rate near human H3K4me3 is much lower — about half the rate that the comparisons with non-human primates revealed. So the authors speculate that …
Taken together, these results suggest that at least a subset of the TSS regions with H3K4me3 enrichment in human (compared to non-human primates) were exposed to evolutionary driven DNA sequence changes on a lineage of the common ancestor of H. sapiens and the archaic hominins, but subsequently were stabilized in more recent human evolution, after splitting from other hominins.
What I like about this research is that the team used real human brain cells. No, not from living people, of course. Cadavers. And they didn’t just grind up a lump of brain in the blender, either. They painstakingly separated prefrontal cortex neurons from glial cells and other types to get at the real differences in the cells that matter, from the brain region that makes executive decisions and fancy associations.
What’s more, they may have sidestepped the problem with dead tissue — sample degradation – by measuring histone methylation. Apparently these marks don’t appear to change much after their host has died.
What I don’t like about the study is pretty standard. The human brain samples came from only 11 subjects — seven children and four adults.
The research team focused only on H3K4me3 peaks that all the humans had in common, so although they might’ve missed some peaks, it’s not that bad of a shortcoming. But there’s also the problem that the human subjects’ brains had already developed — as the authors hint in their discussion, fetal neuronal gene regulation could hold many of the important secrets, since the period of actual brain development is when you’ll probably find a lot of human-specific differences.
I’m anxious to see more of these kinds of studies, and I bet they’re in the works right this minute. It seems that there’s finally a big enough set of lab tools to get at the nitty-gritty parts of big questions.
[Flickr user IsaacMao's picture "Child Brain" is used here under a Creative Commons license.]
Shulha HP, Crisci JL, Reshetov D, Tushir JS, Cheung I, Bharadwaj R, Chou HJ, Houston IB, Peter CJ, Mitchell AC, Yao WD, Myers RH, Chen JF, Preuss TM, Rogaev EI, Jensen JD, Weng Z, & Akbarian S (2012). Human-specific histone methylation signatures at transcription start sites in prefrontal neurons. PLoS biology, 10 (11) PMID: 23185133
When it comes to acetylation and epigenetics your mind probably goes right to histones. Acetylated histones are associated with relaxed, transcriptionally active DNA. However, acetylation is an important post-translational modification of lysine in many cellular proteins. It is as widespread as phosphorylation. It is reversable. Functionally, acetylation is known to be involved in the effects of calorie restriction on metabolism and aging. Now the first direct evidence of a mechanism underlying this process has been reported.
The journal Molecular Cell has recently published Calorie Restriction and SIRT3 Trigger Global Reprogramming of the Mitochondrial Protein Acetylome, authored by scientists from the University of Wisconsin-Madison and the University of Tokyo. They used model mice with age-related hearing loss for this study. This hearing loss is prevented by calorie restriction (CR). They explored the liver mitochondrial protein acetylome by developing a new quantitative, acetyl-proteomic method. The Sirtuin family of deacetylases were already linked to CR. And Sirtuin3 was recently shown to be induced during CR. So the researchers explored the regulatory role of tSIRT3 during CR. They identified multiple pathways where SIRT3 is involved in reprogramming mitochondria during CR via acetylation. Interestingly for “Epiexperts”, among those ID’d were mitochondria DNA expression and maintenance pathways. Part of that SIRT3 led CR reprogramming, is through regulation of mtDNA transcription factors, mtRNA polymerases and mitochondrial ribosome proteins. Please see Table 1. in the pub for the list of SIRT3 targets in this functional group. The reprogramming during CR of these targets leads to enhanced mtDNA transciption, mtDNA translation and protein quality control.
Recall, mitochondria function to produce ATP from sugar and oxygen, powering the cell. This process also creates oxidative free radicals that contribute to aging. Mitochondria have their own DNA and can make their own proteins. During calorie restriction, mitochondria performance is actually enhanced. They use less oxygen and produce less damaging free radicals. Again, in the model mice this results in prevention of hearing loss.
This is a great paper worth reading. Mainly because it establishes that SIRT3, (of the sirtuins deacetylases family) is directly linked to anti-aging effects. But also because it shows SIRT3 is potentially a significant regulator of mitochondrial epigenetics. It’s like by eating less, SIRT3 directs mitochondria to become environmentally friendly power stations with high energy efficiency ratings.
Hebert AS, Dittenhafer-Reed KE, Yu W, Bailey DJ, Selen ES, Boersma MD, Carson JJ, Tonelli M, Balloon AJ, Higbee AJ, Westphall MS, Pagliarini DJ, Prolla TA, Assadi-Porter F, Roy S, Denu JM, & Coon JJ (2012). Calorie Restriction and SIRT3 Trigger Global Reprogramming of the Mitochondrial Protein Acetylome. Molecular cell PMID: 23201123
Microbiologists rushed to respond to the 2011 pathogenic E.coli (0104:H4) outbreak in Europe. The new strain’s DNA was sequenced within 3 days time. The trace back investigation identified an organic bean sprouts field as the source. Now, Pacific Biosciences with collaboration from New England Biolabs, reports Genome-wide mapping of methylated adenine residues in pathogenic Escherichia coli using single-molecule real-time sequencing in the journal, Nature Biotechnology (open access paper).
Epigenetic analysis reveals the potential for restriction modification methyltransferase enzymes (RM MTases) to have important roles in this pathogenic phenotype. 0104:H4 phenotype virulence has been defined by its production of high levels of Shiga toxin. AND it turns out that this strain has specific MTases that can promote that production.
SMRT sequencing was used to simultaneously map both the E.coli DNA sequence and strand-specific methylation patterns, yielding functional information. From this data sequence motifs for strain specific methyltransferase enzymes were deduced. New MTase activities were ID’d by correlating the methylation patterns with transcriptome profiles. The functions of these MTases were probed. In one experiment when a phage encoding both the shiga toxin and an 0104:H4 MTase was incorporated into the genome of a non-pathogenic E.coli strain, 1/3 of its transcriptome changed and it was able to produce the Shiga toxin. In another experiment, knocking out a 0104:H4 specific MTase from the strain showed significant epigenetic changes affecting multiple systems.
It’s impressive how the third generation SMRT sequencing technology can be applied to discovering bacterial epigenetic processes key to establishing pathogenicity. Hopefully these techniques will enable the development of new medicines for hemorrhagic colitis and hemolytic uremic syndromes to save lives!
Fang G, Munera D, Friedman DI, Mandlik A, Chao MC, Banerjee O, Feng Z, Losic B, Mahajan MC, Jabado OJ, Deikus G, Clark TA, Luong K, Murray IA, Davis BM, Keren-Paz A, Chess A, Roberts RJ, Korlach J, Turner SW, Kumar V, Waldor MK, & Schadt EE (2012). Genome-wide mapping of methylated adenine residues in pathogenic Escherichia coli using single-molecule real-time sequencing. Nature biotechnology PMID: 23138224
The most recent pub from the stream of research put forth by New England Biolabs scientists, is a collaboration with scientists from Pacific Biosciences™ . See this open access paper Iain A. Murray et al. The methylomes of six bacteria. (2012) Nucleic Acids Research. It demonstrates how the 3rd generation SMRT DNA sequencing system is used to explore bacterial methylomes. Many exciting discoveries about microbe epigenetic systems are sure to follow this technological advance!
So why is DNA methylated in bacteria? Mainly it functions as part of restriction modification systems. But bacterial methyltransferases also take part in gene expression, host-pathogen interactions, DNA damage, and DNA repair. Microbe methylation modifications include N6-methyladenine (6-mA), N4-methylcytosine (4-mC) & 5-methylcytosine (5-mC).
Single-molecule, real-time sequencing, or SMRT, analyzes DNA as it is sequenced by collecting light pulses emitted as a byproduct of labelled nucleotide incorporation. Algorithmic analysis is subtle enough to detect certain base modifications. A caveat to methylation analysis is that 5-mC is still a bit too subtle. However, for this study, associated methyltransferase genes were cloned and analyzed separately, where appropriate, to ID 5mC sites. The researchers were able to perform methyltransferase (MTase) recognition motif analysis. The recent upgrade of the PacBio® RS High Resolution Genetic Analyzer software also made this project possible.
Richard Roberts, Ph.D., New England Biolab’s Chief Scientific Officer, and senior author on the paper, commented: “DNA methylation is widespread in bacteria where it can protect against restriction enzymes and also regulate gene expression. Until the advent of SMRT sequencing it was not possible to examine the complete methylome of any bacterium. Now it has become simple and we are awash in fascinating new data. Understanding the biological significance of these methylation patterns represents a welcome new challenge for microbiologists.”
I’m sure all you Epiexperts are just as keen to see how the data on microbe gene expression, controlling functions like adaptability and disease pathology, plays out.
Murray IA, Clark TA, Morgan RD, Boitano M, Anton BP, Luong K, Fomenkov A, Turner SW, Korlach J, & Roberts RJ (2012). The methylomes of six bacteria. Nucleic acids research PMID: 23034806
First of all, a hearty congratulations to Dr. Shinya Yamanaka and Dr. John Gurdon for winning this year’s Nobel prize for Medicine, for their discoveries that adult cells could be transformed back to embryonic-like states. Recently, Dr. Yamanaka has publicly warned of dangerous “stem cell therapies” currently offered in various countries, without any pre-clinical testing in animals. This was an important message considering possible tragedies, both for any patients desperate for a cure, who end up sick or dead…and for the public, who might lose their trust in potential future stem cell therapies developed safely under strict scientific methods.
Induced pluripotent stem cells (iPSCs) can be transformed from somatic cells, through the expression of only four transcription factors, using Kyoto University viral delivery methods. However, its been shown that the process of reprogramming these cells results in genetic and epigenetic aberrations in comparison to embryonic or parental somatic cells. Other methods also have been developed, or are in development, to produce IPSCs. For example protein-induced pluripotent stem cells. Goals for any method include producing non-tumorigenic, completely reprogrammed cells
For the recent pub, Sergio Ruiz & Dinh Diep et al. Identification of a specific reprogramming-associated epigenetic signature in human induced pluripotent stem cells. (2012) PNAS, the authors developed a method to discriminate between hESCs and hiPSCs based on targeted bisulfite sequencing with padlock probes, to produce unbiased hierarchical clustering of global methylation. Interestingly, higher reprogramming efficiency was associated with less difference in methylated CpG sites between somatic and iPSC cells. Methylation changes at only nine genes amongst all the iPSC cell lines, regardless of origin cell type. The epigenetic signature for segregation was made clear because areas of lower CgP content were covered. Previous analysis by restricted representation bisulfite sequencing (RRBS), which focuses on CpG islands, could not differentiate between ESCs and iPSCs in this way. The caveat is that more cell lines need to be tested to enhance this epigenetic signature’s utility.
Ruiz S, Diep D, Gore A, Panopoulos AD, Montserrat N, Plongthongkum N, Kumar S, Fung HL, Giorgetti A, Bilic J, Batchelder EM, Zaehres H, Kan NG, Schöler HR, Mercola M, Zhang K, & Izpisua Belmonte JC (2012). Identification of a specific reprogramming-associated epigenetic signature in human induced pluripotent stem cells. Proceedings of the National Academy of Sciences of the United States of America, 109 (40), 16196-201 PMID: 22991473
Sure, M.D.s often suffer a lot of pressure. But as I learned in a brief hospital job, nurses really bear the brunt of all the biological clean-up, red tape, weird hours, patient complaints, and snippy doctors’ demands. So this new study in PLoS One on stress-related epigenetic changes in shift-working female nurses really caught my attention, and seemed like a good followup that post on situational stress and epigenetics. Nurses under high stress appear to have their gene expression epigenetically regulated in a way that may decrease serotonin in the brain’s synapses. It seems a bit like the reverse of Prozac, and it bears a passing resemblance to what might happen at the beginning of depression.
By interfering with serotonin transporter proteins, Prozac and other SSRI drugs allow the “well-being” neurotransmitter serotonin to exert its effects on recipient neuron for a little longer. But according to this study by Jukka Alasaari and Tiina Paunio at the National Institute for Health and Welfare in Helsinki, Finland — and colleagues — high stress appears to trigger less promoter methylation of the serotonin transporter gene, SLC6A4. That usually means cellular machinery makes more mRNA from a gene, and as a result, expresses it more fully. So: more stress, more serotonin transporter, less serotonin the synapses.
I’d expect our physiology to compensate stress, but that’s often not how it works. From the authors’ citations, here’s another example of high stress leading to low serotonin transporter-gene methylation. Alasaari and Paunio discuss it this way:
In the context of this study, we hypothesize that hypomethylation of SLC6A4 presents an adaptational mechanism for stress. While this adaptation is physiological and initially serves to maintain the individual’s best possible functional capacity during stress, it might, eventually, increase risk for functional disturbances, such as decreased cognitive ability and depressed mood, simultaneously with failure of other coping mechanisms. Interestingly, relative lack of serotonin in brain is one of the major hypotheses of depressive disorder, and serotonin transporter is known to be one of the major targets of many antidepressants, including the selective serotonin re-uptake inhibitors .
So maybe we’re talking about the first steps in the route to disease, although I don’t understand how increased serotonin re-uptake is helpful when you’re stressed.
But back to the experiments themselves. The authors chose the high- and low-stress extremes from among a large (n=5615) group of nurses who answered questionnaires based on Karasek’s Model, in which people in high-stress environments report high work demands and low control over the situation, while people under low stress report low demands and high control. The 49 remaining nurses also answered surveys about burnout and non-clinical depression, with about half of the high-stress group showing signs of burnout and at least mild depression. Not surprisingly, the low-stress group displayed few such signals — only two people with mild depression.
Thereafter, the researchers used bisulfite sequencing to test the nurses’ blood for the methylation of five CpG sites in the serotonin transporter’s promoter. And after a fair amount of statistical work, discovered a significant association between the high-stress group and low promoter methylation.
But oh no. We’re talking about testing blood, and we’re speculating about things that happen in the brain. And so it’s time to talk about caveats. But at least the authors were nice enough to mention the same ones I came up with.
The research relies on peripheral blood leukocyte samples as a proxy for neurons, which are ethically unreachable. (In Soviet Union, proxy relies on you.) No one really knows if the gene methylation in these two types of cells is similar — we’re assuming that’s the case until proven otherwise. And yes, I simplified the role of serotonin above. It’s associated with feelings of well-being when we’re talking about its role in the brain, but it has a variety of other roles elsewhere in the body.
And a couple more caveats: This study is small, with 49 subjects — 24 nurses from high-stress environments and 25 from relatively low-stress environments — partly because the investigators removed a lot of participants to control for smoking and alcohol consumption. Finally, the study relies on a bisulfite sequencing protocol to detect methylation, which means that inconsistent PCR amplification could have skewed the results. The team validated its findings by following up with an array-based method, but it’s important to note these things.
Still, that’s science. And without a few tentative steps steps forward, where would we be? Even more stressed, that’s where.
[I was stumped about how to portray both nurses and stress, or highly stressed nurses, so I opted for the pic above, Italian Nurses, which is by Flickr user jdlasica and is reproduced here under a Creative Commons license.]
Jukka S. Alasaari1, Markus Lagus1, Hanna M. Ollila1, Auli Toivola1, Mika Kivima ̈ki2,3, Jussi Vahtera2,3,, & Erkki Kronholm4, Mikko Ha ̈rma ̈2, Sampsa Puttonen2, Tiina Paunio1,5* (2012). Environmental Stress Affects DNA Methylation of a CpG Rich Promoter Region of Serotonin Transporter Gene in a Nurse Cohort PLoS One, 7 (9) DOI: 10.1371/journal.pone.0045813
Yu Bo is a highly respected, world famous chef who prepares modern versions of Chinese cuisine. His dishes are terrifically creative in their presentation of traditional Cheng Du providence flavors. Yu Bo’s process reveals the ‘essence’ of a dish, displaying it through modern culinary procedures and techniques.
This inventive process is similar to how biological information can be processed to reveal an essential disease profile. Breast cancer has many known associated single-nucleotide polymorphisms(SNPs). Most do not disrupt coding gene sequences. How can we discover which are causing disease?
Because exhaustive functional analysis of all GWAS results just doesn’t make sense, Richard Cowper-Sal-lari et al Breast cancer risk-associated SNPs modulate the affinity of chromatin for FOXA1 and alter gene expression (2012) Nature Genetics, propose the use of a new “integrative functional genomics” approach to explore relationships between breast cancer-associated SNPs and, as the authors phrase it, “…cistromes and epigenomes (that) lie at the source of cell identity”. An epigenome and a cistrome are genome-wide sets of epigenetic marks and transcription factor binding sites, for a specific cell type and cellular environment.
Integrative functional genomics works through a computational method called variant set enrichment (VSE) – followed by a second computational method termed Intragenomic replicates (IGR) to predict affinity of a binding motif based on a SNP sequence. The results are quite elegant. They show that the majority of risk-associated SNPs function to modulate the pioneer factor FOXA1, whose binding is necessary to alter the structure around genes to grant access for the transcription factor ESRI (estrogen receptor α).
My complements to the chefs!
Cowper-Sal Lari R, Zhang X, Wright JB, Bailey SD, Cole MD, Eeckhoute J, Moore JH, & Lupien M (2012). Breast cancer risk-associated SNPs modulate the affinity of chromatin for FOXA1 and alter gene expression. Nature genetics PMID: 23001124
It seems like every article about epigenetics in the popular press includes a sentence about how maybe, just maybe this new finding or other proves that Jean-Baptiste Lamarck was right some 200 years ago. He famously tied “acquired traits” — characteristics an individual accumulates during its life, such as muscular arms — into a broader theory of how species evolve.
The most recent version I’ve seen is in the Sept 8 New York Times opinion piece “Why Fathers Really Matter,” though it’s indirect and noncommittal, as Lamarck comparisons tend to be:
Epigenetics proves that we are the products of history, public as well as private, in parts of us that are so intimately ours that few people ever imagined that history could reach them. (One person who did imagine it is the French 18th-century naturalist Jean-Baptiste Lamarck, who believed that acquired traits could be inherited. Twentieth-century Darwinian genetics dismissed Lamarckism as laughable, but because of epigenetics, Lamarckism is staging a comeback.)
Does “staging a comeback” imply that Lamarck may have been right? Writer Judith Schulevitz leaves that as an exercise for the reader. (I mean, she’s careful not to make any concrete statements.) The rest of the article is a fairly interesting rundown of some interesting epigenetic effects — low calorie intake and heart disease rates, that kind of thing.
But about Lamarck: No, he was wrong.
Sure, you can have a higher risk of diabetes if your father ate a high-calorie diet before your were born, but that doesn’t mean that diabetes is adaptive to a high-food environment. Also, give it a couple generations, and without more of the same environmental stimuli, the epigenetic effects fade away. And there’s no evidence that epigenetic effects are additive in any way: could you use one epigenetic effect to increase your clan’s risk of diabetes generation after generation? Probably not, since there’s a limited amount of epigenetic modification, say DNA methylation, that a single gene — or set of genes — can accommodate.
alling epigenetics evidence for Lamarckian evolution is like mistaking a dimmer switch for an electronics technician. So it’s surprising to see that claim repeated so often, for example in this PLoS research article. And in the popular press here, here, and here. (I do like the bonus florid prose in that second one from The New Republic: “Epigenetic research suggests that organisms adapt much more quickly and in much more promiscuous conversation with their habitats than orthodox theories of natural selection allow for.”)
Still, let’s not forget what Lamarck got right. It’s true that the environment changes the physiology of organisms permanently over generations — just not directly, and not over just a couple generations. His evolutionary theory was apparently the first to lay out a coherent overall story that relied on natural laws, rather than miracles and magical thinking.
This step toward finding the natural mechanisms governing life played a major role in inspiring Charles Darwin and many more Enlightenment naturalists. Besides, the man named thousands of species, many of which still bear his name, like the blue jellyfish Cyanea lamarckii.
It’s a shame Lamarck isn’t appreciated for his real contributions, but that’s no reason to get all misty-eyed about his mistakes.
[Lamarck's statue in the picture above sits in Paris's Jardin des Plantes. The picture can be found here at Wikimedia Commons, and it's used on this page under a Creative Commons license.]
[Similarly, the blue jellyfish picture is from Wikimedia Commons, here. It's also used in this post under a Creative Commons license.]
Ou X, Zhang Y, Xu C, Lin X, Zang Q, Zhuang T, Jiang L, von Wettstein D, & Liu B (2012). Transgenerational Inheritance of Modified DNA Methylation Patterns and Enhanced Tolerance Induced by Heavy Metal Stress in Rice (Oryza sativa L.). PloS one, 7 (9) PMID: 22984395