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Wondering if there is a place that has a list/table/database of all the genes in the human genome, and/or all the known genes in all the species we've studied so far. Something that contains any of this would be great.
I found this but not sure yet if that is just for humans and just for one chromosome. But I'd like something along those lines across species, or the closest thing to that that exists.
In principle there are a LOT of these databases and depending on your specific questions you may want to look into different ones. Like already mentioned NCBI hosts basically all of the available information, however it's not always easy to find the bits you care about.
The database I personally use the most is biomart (hosted by the ensembl consortium). It doesn't just contain all known for genes for pretty much all organisms, but is also able to link this to a ot of different information sources.
I usually access the database directly via the biomaRt R package, so I can't really say how good the actual website this. However, this link should allow you to download a table of all human genes with names, (unique) identifies & descriptions (I selected these from the 'Attributes' section).
ReXSpecies – a tool for the analysis of the evolution of gene regulation across species
Annotated phylogenetic trees that display the evolution of transcription factor binding in regulatory regions are useful for e.g. 1) narrowing down true positive predicted binding sites, providing predictions for binding sites that can be tested experimentally, and 2) giving insight into the evolution of gene regulation and regulatory networks.
We describe ReXSpecies, a web-server that processes the sequence information of a regulatory region for multiple species and associated (predicted) transcription factor binding sites into two figures: a) An annotated alignment of sequence and binding sites, consolidated and filtered for ease of use, and b) an annotated tree labeled by the gain and loss of binding sites, where the tree can be calculated from the data or taken from a trusted taxonomy, and the labels are calculated based on standard or Dollo parsimony. For genes involved in mammalian pluripotency, ReXSpecies trees highlight useful patterns of transcription factor binding site gain and loss, e.g. for the Oct and Sox group of factors in the 3' untranslated region of the cystic fibrosis transmembrane conductance regulator gene, which closely match experimental data.
ReXSpecies post-processes the information provided by transcription factor binding site prediction tools, in order to compare data from many species. The tool eases visualization and successive interpretation of transcription factor binding data in an evolutionary context. The ReXSpecies URL can be found in the Availability and requirements section.
- Department of Entomology and Nematology, Center for Population Biology, University of California, Davis, Davis, CA, United States
Genes limited to particular clades, taxonomically restricted genes (TRGs), are common in all sequenced genomes. TRGs have recently become associated with the evolution of novelty, as numerous studies across the tree of life have now linked expression of TRGs with novel phenotypes. However, TRGs that underlie ancient lineage specific traits have been largely omitted from discussions of the general importance of TRGs. Here it is argued that when all TRGs are considered, it is apparent that TRGs are fundamental to biology and evolution and likely play many complementary roles to the better understood toolkit genes. Genes underlying photosynthesis and skeletons, for example, are examples of commonplace fundamental TRGs. Essentially, although basic cell biology has a highly conserved genetic basis across the tree of life, most major clades also have lineage specific traits central to their biology and these traits are often based on TRGs. In short, toolkit genes underlie what is conserved across organisms, while TRGs define in many cases what is unique. An appreciation of the importance of TRGs will improve our understanding of evolution by triggering the study of neglected topics in which TRGs are of paramount importance.
Finally, A Map Of All The Microbes On Your Body
Scientists Wednesday unveiled the first catalog of the bacteria, viruses and other microorganisms that populate every nook and cranny of the human body.
Researchers hope the advance marks an important step towards understanding how microbes help make humans human.
The human body contains about 100 trillion cells, but only maybe one in 10 of those cells is actually — human. The rest are from bacteria, viruses and other microorganisms.
"The human we see in the mirror is made up of more microbes than human," said Lita Proctor of the National Institutes of Health, who's leading the Human Microbiome Project.
"The definition of a human microbiome is all the microbial microbes that live in and on our bodies but also all the genes — all the metabolic capabilities they bring to supporting human health," she said.
These microbes aren't just along for the ride. They're there for a reason. We have a symbiotic relationship with them — we give them a place to live, and they help keep us alive.
"They belong in and on our bodies they help support our health they help digest our food and provide many kinds of protective mechanisms for human health," Protor said.
Microbes extract vitamins and other nutrients we need to survive, teach our immune systems how to recognize dangerous invaders and even produce helpful anti-inflammatory compounds and chemicals that fight off other bugs that could make us sick.
"These microbes are part of our evolution. As far as we can tell, they are very important in human health and probably very important in human disease as well," said Martin Blaser of New York University.
These bugs generally don't make us sick. But when we disrupt the delicate ecosystems they carefully construct in different parts of our bodies, scientists think that can make us sick.
"There can be a disturbance in the immune system. There can become some kind of imbalance. And then you can get a microorganism which, under normal circumstances, lives in a benign way and can become a disease-bearing organism," Proctor said.
Taking too many antibiotics, our obsession with cleanliness and even maybe the increase in babies being delivered by Caesarean section may disrupt the normal microbiome, she said.
So the idea behind the micobiome project was to get the first map of what a normal, healthy microbiome looks like.
More than 200 scientists spent five years analyzing samples from more than 200 healthy adults. The samples came from 18 different places on their bodies, including their mouths, noses, guts, behind each ear and inside each elbow.
"This is the only study to date anywhere in the world where peoples' microbiomes across a human body were sampled and analyzed. Here was an effort to really investigate the full landscape, if you will, of the human microbiome across the body," Proctor said.
Scientists identified some 10,000 species of microbes, including many never seen before, according to the first wave of results, which are being published in 16 papers in the journals Nature and PLoS.
"This is like going into uncharted territory — going into a forest and finding a new species of butterfly or new type of mammal or something like that — a new kind of bird," said George Weinstock of Washington University in St. Louis.
Those 10,000 or so species have more than 8 million genes, which is more than 300 times the number of human genes.
And scientists found some very interesting things when comparing microbiomes.
"People were very different from each other, but skin was more like skin and gut was more like gut. So the composition of microbes and the kinds of genes that they have are very much habitat-specific," Proctor said.
Now that scientists have an idea of what a healthy microbiome looks like, they can start to explore this super-organism — this complex mishmash of human and microbial cells.
"How do they talk to our human cells? And how do human cells talk back to them? Because it's really a concert that they're playing together, and that's what makes us who we are," Weinstock said.
Scientists have already discovered some intriguing clues. For example, the microbes in a pregnant woman's birth canal start to change just before she gives birth. Scientists think that's so their babies are born with just the right microbiome they'll need to live long, healthy lives.
Using WGBS, we generated one of the first large-scale, single-nucleotide resolution cattle somatic tissue methylomes. Cattle-unique tissue-like rumen was also reported for the first time. The global CG methylation levels detected ranged from 72.8 to 78.1% among our cattle samples, which were similar to those in other mammalian species like humans (
70%)  and what we reported previously . Our genome-wide cattle methylomes confirmed existing knowledge that DNA methylation is important for gene expression and plays a critical role in tissue-specific processes [5, 60]. In promoter regions, DNA methylation is associated with transcriptional repression whereas in gene bodies, DNA methylation is generally enriched in the body of highly transcribed genes [61,62,63,64]. We tested the impacts of genome assembly quality on read mapping and DNA methylation calling, revealing DNA methylation peaks and valleys did change their locations and magnitudes, especially when they are near chromosome ends and sudden drops.
In this study, we reported large-scale PMDs in multiple cattle tissues. We then cross-referenced them on the chromosome level with CpG, genes, transcriptions, HMRs, histone codes, satellites, and TADs. We found that cattle PMDs share features with those identified in other species, especially those identified in human tissues: localization in genomic regions with low GC contents, low CGI density, low gene density, and lack of active histone marks. Although PMDs have been associated with gene repression and inactive chromatin marks, genes within tissue-specific PMDs did display tissue-specific functions. Previous human results show that PMDs are established within preformed TAD B compartments after cell lineage decision in cardiac myocytes . The higher order chromatin conformation is proposed to be a regulatory mechanism guiding cell type-specific establishment of CpG methylation and non-CpG methylation signatures, like PMDs in TAD B compartments and HMR in TAD A compartments, respectively. Similarly, the endogenous bovine Hi-C contact maps uncovered that TAD B compartments were often associated with PMDs in the cattle genome. Thus, we hypothesize that a similar silencing mechanism may operate in cattle PMDs during cattle tissue specification and development.
We detected large differences between cattle somatic tissues in terms of HMRs. For example, the peak size of non-TSS-HMR for the placenta was significantly larger than those in sperm and normal tissues, while the peak sizes of TSS-HMR were highly consistent, (
2000 bp) among all tissue (Fig. 3a). This might indicate the dramatic difference of the placenta as compared to the sperm and other somatic tissues and the importance of the TSS-HMR throughout all tissues. We also classified genes into 5 groups according to their promoter location relative to the TSS-HMR and studied their potential impacts on gene regulation and genome evolution. By performing correlation analyses between the paired genes’ expressions, we found the paired genes (twin-genes) within TSS-HMR T2 would have more chances to be co-expressed (Fig. 4d). Moreover, our results showed that those paired genes were more consistent across mammalian species. As for genes within the TSS-HMR T3, i.e., with variable TSS or promoters, we found that they had a high possibility of being regulated by tissue-specific methylation of TSS-HMR. We used WGCNA to study gene networks based on pairwise correlations between their expressions and identified tissue-specific genes related to tissue functions. Combining with the gene expression using the RNA-seq data, we found 32 genes’ tissue-specific HMRs were highly correlated with their expression. The tissue-specific TSS-HMRs were greatly enriched for putative binding sites of transcription factors, which are known to have tissue-specific function (Fig. 4i). Combined with gene expression using the RNA-seq data, we identified tissue-specific gene expression correlated with tissue-specific HMR. Additionally, using our WGBS data, we totally identified 50,023 eCGIs at a single-base resolution and validated 42.24% of the total cCGI.
In germ cells like sperm, common repeats are normally highly methylated. The conserved piRNA pathway has been proposed to be important for recognizing and silencing repeats in germ cells . However, we still found more than expected HMRs that overlapped common repeats, suggesting some individual elements can evade piRNA-based silencing. Examining patterns of HMR-associated repeats is very informative. One possibility is that just like genes, young repeats contain promoters or regulatory regions and/or their TF binding and transcription activation can facilitate their evading default methylation. Although most of Bov-A2 elements follow the normal expectation, showing a negative correlation between methylation level and age (represented by their divergence from its consensus sequence), we detected that some Bov-A2 elements were hypomethylated in cattle sperm cells. Similar to the young Alu subfamilies, which introduce binding sites for transcription factor SABP in human sperm [67, 68], we found some Bov-A2 elements inserted into genes like NME8 and PHX4 that function in spermatogenesis or transcription regulation. Through examining these Bov-A2 insertions, we found the binding sites for multiple AZF1 (azoospermia factor 1), which have an essential meiotic function in fly and human spermatogenesis . Diseases associated with AZF1 include azoospermia and varicocele . As the introduction of TFBS by active Bov-A2 insertions could change the promoter structure, we hypothesize that Bov-A2 insertions in sperm cells may be involved in specific regulation of functional genes.
Future directions and limitations
Genome editing technologies, CRISPR/Cas9, can directly target and edit individual methylation sites and therefore determine the exact function of DNA methylation at a specific site, as reviewed recently . It is noted that because our data were produced from bulk cells, we were unable to determine the impact of cell composition on our results. Based on 64 human reference cell types, the human GTEx Consortium recently used the xCell method  to characterize the effect of cell type heterogeneity on analyses from bulk tissue . Estimated cell type abundances from bulk RNA-seq across tissues reveal the cellular specificity of genetic regulation of gene expression across human tissues . Due to limited resources, such as cattle reference cell types, future studies will be warranted to test these hypotheses and estimate their effects.
In summary, using conventional WGBS and RNA-seq, we provided baseline methylation and transcription profiles for cattle somatic cells at a single-base resolution. We characterized the DNA methylome and assessed DNA methylation patterns. We reported rich data sets of PMDs and HMRs across different tissues and detected that some of them were correlated with tissue development. Our study contributes to the understanding of cattle DNA methylation patterns and provides foundational information for further investigations.
10 Unusual Genetic Mutations in Humans
No two people are alike, due to the subtly different ways our genomes are expressed. But sometimes these biological differences lead to genetic mutations that are extremely rare, and sometimes debilitating. Historically, many people suffering from these mutations were labeled monsters or freaks — but today, we know they are simply part of the broad spectrum of genetic variations in our species. Here are 10 of the most unusual genetic mutations we've identified in humans.
This genetic disorder is as rare as it is severe. The classic form of the disease, called Hutchinson-Gilford Progeria, causes accelerated aging.
Most children who have progeria essentially die of age-related diseases around the age of 13 , but some can live into their 20s. Death is typically caused by a heart attack or stroke. It affects as few as one per eight million live births .
The disease is caused by a mutation in the LMNA gene, a protein that provides support to the cell nucleus. Other symptoms of progeria include rigid (sclerotic) skin, full body baldness (alopecia), bone abnormalities, growth impairment, and a characteristic “sculptured” nasal tip.
Progeria is of great interest to gerontologists who hope connect genetic factors to the aging process. Image: HBO.
2. Uner Tan Syndrome
Uner Tan syndrome is a somewhat controversial condition, whose most obvious property is that people who suffer from it walk on all fours. UTS is a syndrome that was proposed by the Turkish evolutionary biologist Üner Tan after studying five members of the Ulaş family in rural Turkey. These individuals walk with a quadrupedal locomotion, use primitive speech, and have a congenital brain impairment (including “disturbed conscious experience”). The family was featured in a 2006 BBC2 documentary called, " The Family That Walks On All Fours ." Tan describes it like this:
The genetic nature of this syndrome suggests a backward stage in human evolution, which is most probably caused by a genetic mutation, rendering, in turn, the transition from quadrupedality to bipedality. This would then be consistent with theories of punctuated evolution.
The new syndrome, says Tan, “may be used as a live model for human evolution.” Some experts think this is bunk, and that genetics may have very little to do with it.
Hypertrichosi s is also called “werewolf syndrome” or Ambras syndrome, and it affects as few as one in a billion people and in fact, only 50 cases have been documented since the Middle Ages.
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People with hypertrichosis have excessive hair on the shoulders, face, and ears. Studies have implicated it to a rearrangement of chromosome 8. It happens due to a disruption of the “crosstalk” between the epidermis and the dermis as hair follicles form in the 3-month fetus at the eyebrows and down to the toes. Normally, signals from the dermis send the messages to form follicles. As a follicle forms, it sends signals to prevent the area around it from also becoming a follicle, which results in the equal spacing of our five million or so follicles. Most of our body parts ignore the messages to form follicles, which explains why most of us are relatively hairless.
4. Epidermodysplasia Verruciformis
Epidermodysplasia verruciformis is an extremely rare disorder that makes people prone to widespread human papillomavirus (HPV) infection. This infection causes scaly macules and papules ( cutaneous squamous cell carcinomas ) to grow on the hands, feet, and even face. These skin “eruptions” appear as wart-like lesions — and even wood-like and horn-like growths — with reddish-brown pigmented plaques. Typically, the skin tumors start to emerge in people between the age of 20 and 40, and the growths tend to appear on areas exposed to the sun. Also called Lewandowsky-Lutz dysplasia, there is no known cure, though treatments to scale back the growths are possible.
The disorder was brought to the public’s attention in November 2007 when a video of a 34-year-old Indonesian man named Dede Koswara appeared on the internet . In 2008, he underwent surgery to have 13 pounds (6 kg) of the warts removed . After the lesions and horns were extracted from his hands, head, torso, and feet, his hands were grafted with new skin. In all, about 95% of the warts were removed.
List of genes across species (or just for humans) - Biology
Mechanisms: the processes of evolution
Evolution is the process by which modern organisms have descended from ancient ancestors. Evolution is responsible for both the remarkable similarities we see across all life and the amazing diversity of that life but exactly how does it work?
Fundamental to the process is genetic variation upon which selective forces can act in order for evolution to occur. This section examines the mechanisms of evolution focusing on:
- and the genetic differences that are heritable and passed on to the next generation
Mutation, migration (gene flow), genetic drift, and natural selection as mechanisms of change
The random nature of genetic drift and the effects of a reduction in genetic variation
How variation, differential reproduction, and heredity result in evolution by natural selection and
How different species can affect each other's evolution through coevolution.
The Continuing Evolution of Genes
Each of us carries just over 20,000 genes that encode everything from the keratin in our hair down to the muscle fibers in our toes. It’s no great mystery where our own genes came from: our parents bequeathed them to us. And our parents, in turn, got their genes from their parents.
But where along that genealogical line did each of those 20,000 protein-coding genes get its start?
That question has hung over the science of genetics ever since its dawn a century ago. “It’s a basic question of life: how evolution generates novelty,” said Diethard Tautz of the Max Planck Institute for Evolutionary Biology in Plön, Germany.
New studies are now bringing the answer into focus. Some of our genes are immensely old, perhaps dating all the way back to the earliest chapters of life on earth.
But a surprising number of genes emerged more recently — many in just the past few million years. The youngest evolved after our own species broke off from our cousins, the apes.
Scientists are finding that new genes come into being at an unexpectedly fast clip. And once they evolve, they can quickly take on essential functions. Investigating how new genes become so important may help scientists understand the role they may play in diseases like cancer.
“It’s premature to make any grandiose claims, but there’s a coherence that’s emerging,” said David Begun, an evolution scientist at the University of California, Davis.
Identifying Gene Families
Scientists first speculated about the origin of genes in the early 20th century. Some proposed that when cells duplicate their DNA, they accidentally copy some genes twice. At first the two genes are identical. But later, they evolve into different sequences.
At the end of the century, as geneticists gained the ability to read the precise sequence of DNA, they found that this hunch was correct. “It became clear that gene duplication played a role in evolution,” Dr. Tautz said.
As genes duplicate over millions of years, they can grow into so-called gene families, each containing hundreds of similar genes.
Podcast: The Origin of Genes, an Antibiotic Overload, Roommate Math
One family, for example, is essential for our sense of smell. These genes encode 390 different kinds of proteins produced in our noses, called olfactory receptors. Each olfactory receptor has a slightly different structure, allowing it to capture a different set of molecules.
Over long periods of evolutionary time, some copied genes change drastically — so drastically, in fact, that they take on entirely new tasks.
Consider hemoglobin, which stores oxygen in red blood cells for delivery throughout the body. Scientists have found that it belongs to a family of genes that do many different things with oxygen and recent studies suggest that it evolved from proteins that grabbed extra oxygen molecules inside cells before they could do harm.
The case for gene duplications became so strong that many scientists grew convinced that it was the source of all new genes. They speculated that when life originally emerged billions of years ago, the first primordial microbes had a tiny set of genes. Those genes then duplicated over and over again to give rise to all the genes on Earth today.
But when scientists gained the ability to sequence entire genomes, there was a surprise waiting for them. They started to find genes that existed in the genome of just one species. According to the duplication theory, these solitary genes shouldn’t exist they would have to have been copied from earlier genes in other organisms.
“They looked like perfectly normal genes, except they were only found in one species,” said Anne-Ruxandra Carvunis, an evolutionary biologist at the University of California, San Diego. “There was no explanation for how a gene could be in one species and not in other ones.”
These genes came to be known as “orphan genes.” As scientists sequenced more genomes, they tried to return these orphans to their gene families. Sometimes they succeeded. But very often the orphans remained orphans.
For some scientists, like Dr. Tautz, the data pointed to an inescapable conclusion: Orphan genes had not been passed down through the generations for billions of years. They had come into existence much later.
“It’s almost like Sherlock Holmes,” said Dr. Tautz, citing the detective’s famous dictum: “When you have eliminated the impossible, whatever remains, however improbable, must be the truth.”
‘De Novo Genes’
Dr. Begun and his colleagues renamed orphan genes “de novo genes,” from the Latin for new. He found that many of his fellow scientists weren’t ready to accept this idea.
“It took a while for people to believe this was occurring,” he said. “It seems kind of nutty to people when they first hear of it.”
One reason it no longer seems so improbable is that Dr. Begun and other researchers have documented the step-by-step process by which a new gene can come into existence.
In many species, ours included, protein-coding genes make up a tiny portion of the genome. New genes can emerge from the vast expanse of noncoding DNA.
The first step is for a tiny bit of DNA to mutate into what scientists call a “start sequence.” All protein-coding genes have start sequences, which enable cells to recognize where genes begin.
Once a cell recognizes the start of a gene, it can make a copy of the gene’s DNA. It can then use that copy as a guide for building a protein.
The new protein may turn out to be toxic, or it may serve no purpose. But once it emerges, new mutations to the new gene may make it more useful.
“Once they’re produced, there’s an opportunity for natural selection to sculpt them,” said Aoife McLysaght, a geneticist at Trinity College Dublin.
Dr. Begun and his colleagues are now getting a look at these early stages in the birth of de novo genes. They can do so by looking for such genes in different populations of a species of the fruit fly Drosophila melanogaster.
The scientists found 142 de novo genes that were present in some populations of flies but not in others, meaning that they must have evolved recently: They’ve had only enough time to spread across part of the species.
Dr. Begun suspects that the true number of de novo genes in the flies is higher. He and his colleagues used very strict guidelines about what stretches of DNA they put on their list, and so they may have missed some genes. “I think we have a lower bound here,” he said.
Dr. Begun’s research indicates that new genes can evolve at a remarkably fast rate — a finding supported by another study, published in the journal eLife.
Christian Schlötterer of the University of Veterinary Medicine in Vienna and his colleagues surveyed five closely related species of Drosophila flies that share a common ancestor that lived about 10 million years ago. The researchers found that as the species diverged from one another, hundreds of new genes evolved along each lineage.
Far from being a fluke, these studies suggest that de novo genes are abundant. In fact, scientists are now wondering why these fast-evolving genes aren’t swelling the genomes of animals and plants.
Dr. Schlötterer and his colleagues found the answer in their study: Along each lineage, many de novo genes are also lost. In some cases, a mutation disables a new gene, so that cells can no longer read them. In other cases, a mutation deletes the entire stretch of DNA where the new gene sits.
While many de novo genes ultimately vanish, some cling to existence and take on essential jobs. Dr. Tautz said the rise of these genes might be as important a factor in evolution as gene duplication.
Some scientists are investigating how that force has shaped our own biology, though it is harder to study de novo genes in humans because many experiments that can be done on flies cannot be done on humans.
Some clues come from diseases. Japanese researchers, for example, have found a de novo gene involved in cancer. The gene, called NCYM, is found only in humans and chimpanzees, suggesting that it arose several million years ago in our common ancestor.
Yusuke Suenaga of the Chiba Cancer Center Research Institute in Japan and his colleagues found that NYCM plays an important role in childhood brain tumors its role in ordinary brain cells remains to be discovered.
NCYM is just one of many de novo genes we carry. Dr. McLysaght and her colleagues estimate there are 40 such genes in the human genome, although other researchers have come up with much higher estimates. But what does that mean to our species? Dr. Carvunis, the evolutionary biologist in San Diego, says the answers may still be far in the future.
“The true impact of de novo genes in what makes us humans,” she said, “remains to be fully investigated.”
List of genes across species (or just for humans) - Biology
In the fruit fly example, some fruit fly larvae were washed up on an island, and speciation started because populations were prevented from interbreeding by geographic isolation. Scientists think that geographic isolation is a common way for the process of speciation to begin: rivers change course, mountains rise, continents drift, organisms migrate, and what was once a continuous population is divided into two or more smaller populations.
It doesn't even need to be a physical barrier like a river that separates two or more groups of organisms it might just be unfavorable habitat between the two populations that keeps them from mating with one another.
Reduction of gene flow
However, speciation might also happen in a population with no specific extrinsic barrier to gene flow. Imagine a situation in which a population extends over a broad geographic range, and mating throughout the population is not random. Individuals in the far west would have zero chance of mating with individuals in the far eastern end of the range. So we have reduced gene flow, but not total isolation. This may or may not be sufficient to cause speciation. Speciation would probably also require different selective pressures at opposite ends of the range, which would alter gene frequencies in groups at different ends of the range so much that they would not be able to mate if they were reunited.
Even in the absence of a geographic barrier, reduced gene flow across a species' range can encourage speciation.
Research Fields in Biology
Science can be a confusing realm – workers in almost all scientific disciplines revel in the fact that they have a huge amount of special terminology, slang and jargon that can confuse and frighten even other scientists. This doesn’t result from any sinister intent, but the concepts under discussion are often so complex that having a simple word that describes a textbook’s worth of ideas becomes really handy. It saves a lot of time and makes sure that everyone is talking about the same thing. Assuming, of course, they know what the word means!
Sadly this means that when researchers come to talk to the pubic, they often get tangled up the complexities of their jargon and forget that not everyone knows what they mean by the ‘Red Queen’, ‘Lamarckism’ or ‘cladistic palaeobiogeography’. This even extends to the names of the fields they work in, so it seemed a good idea to give a list of the more common / simple research fields. Many people probably just think of biology in terms of zoology, botany and medicine, if that, when of course these are exceptionally general terms. Almost all researchers end up specialising in one or more much narrower fields, so although everyone on AAB is a biologist in one sense, I suspect that few would ever describe themselves as such. One person might specialise in how behaviour (ethology) affects big evolutionary changes (macroevolution) in humans (anthropology) and another on how the environment (ecology) influences behaviour (ethology) in fossil insects (palaeontology and entomology). So one looks at 250 million year old grasshoppers and works in a geology museum and the other studies living humans in cities and works in a hospital, but both could be described as ethologists!
Hopefully this list will give you an idea of some of the fields we work in, and what the terms mean.
Biology – essentially the ‘study of life’, and therefore everything to do with life comes under this term. For historical reasons, the term biologist is not usually applied to researchers who happen to specialise in the mammalian species Homo sapiens. Nevertheless, humans are biological beings, and they can be studied using a biological approach.
Botany – the study of plants. Again for historical reasons, this also generally includes fungi, algae and lichens, even though these organisms are no longer technically considered to be plants.
Zoology – the study of animals. Not the study of zoos! Zoo in this term is a contraction of zoological garden, though of course the root word is the same.
Medicine – the study of health. This includes diseases and problems of age, genetic disorders and injuries, etc. Of course thanks to our ‘human-centric’ view, most people will think of medicine as just referring to health in people, though of course we also have veterinary medicine for the study (and practice) of the health of animals.
Palaeontology – the study of extinct life (not to be confused with archaeology which covers only ancient human artefacts like houses or tools). Covers all life (again except humans) but the root term “palaeo-“ (which means “ancient”) is often combined with other key words to provide a more specific description. For example, palaeobotany is the study of extinct plants, and palaeoecology is the study of extinct ecosystems. Just to be confusing it can be spelt palaeontology or paleontology. While the study of rocks (geology) is a separate science, by definition palaeontology involves elements of geology that are needed to study the rocks in which the fossils are found.
Anatomy – the study of the shape and structure of animals and plants. This includes not only gross body structure, but also organs, parts of organs, and even individual cells.
Biochemistry - the study of the chemistry of living organisms – how chemical reactions happen in the body and why. This field has considerable areas of overlap with genetics and physiology.
Biogeography – the study of how life is distributed across the planet. This is especially important in palaeontology, as we can see how animals and plants spread across the world once they had evolved and see how patterns of distribution changed over time.
Biomechanics – this is an area where biology and physics overlap. Biomechanics is the study of how things move or act in a physical world, form how animals run, swim and fly (locomotion) right down to how muscles work, or even how channels in cell membranes open and close, and molecules move.
Developmental Biology – in the past this was more often referred to as embryology (the study of the embryo developing from a cell to an independent organism), but of course ‘development’ covers all manner of organisms. This is becoming increasingly important in biology as new techniques allow us to look in detail at how organisms grow and change, what genes are responsible and how they alter the pattern of development.
Ecology – the study of living things in relation to each other and to their environment. In other words, the study of how organisms live and interact with each other – who eats what, and how much, who gets eaten, and who competes or cooperates with whom.
Ethology – the study of behaviour. How animals behave, and the underlying reasons for their behaviour and how they originated and evolved.
Evolutionary Biology – perhaps the most wide-ranging field in biological sciences, one way or another, evolution touches just about every area of research. Some study evolutionary theory, or how organisms change, why they change, how they are related to others and so on. There is very little that evolution (either through direct action, or the evolutionary history of the organism) does not affect.
Genetics / Molecular Biology – the science of inheritance, how genes are expressed, and the structure and function of biologically important molecules (e.g. proteins).
Marine Biology – the study of sea life, covering elements of other biological fields like zoology, botany, ecology as well as more geographical skills such as studying ocean currents and weather patterns.
Microbiology – the study of microorganisms, defined as organisms that cannot be seen with the naked eye. This normally includes single-celled organisms such as bacteria and some algae, in addition to viruses and prions. A virus is essentially a non-cellular biochemical complex, existing at the boundary of the biological and chemical realms.
Pathology – the study of diseases and how to cure them.
Pharmacology – the study of drugs and medicines and how they affect the (typically human) body.
Physiology – the study of the biological processes. This really goes hand-in-hand with anatomy- knowing how an engine is built may be useful, but it’s also important to know how it works when you turn it on!
Taxonomy – the study of scientific names, or more specifically the science of naming species, making sure each species can be identified properly and working out its evolutionary relationships to other species (this latter part is often termed ‘systematics’).
Of course I could go on (quite a lot!). New fields of research are always being generated through new ideas and concepts, or old areas are combined to give a new approach or overlap. Even most groups of organisms have their own research name - almost everyone has heard the term ornithology for the study of birds, but there is also mammology (mammals), mycology (fungi), malacology (molluscs) and more, and I have not even included these here.
This list should cover the most common ones (if in little detail) that you are likely to encounter or hear about, but if you want to know more about them, or about other research areas, then why not ask us a question?