Reptiles and facultative parthenogenesis

If you understand the title of this post, you have my undying respect. Most people wrongly assume  that asexual reproduction only occurs in prokaryotes and plants, by binary fission or runners for example, however animals can also reproduce in this manner, and not via divine impregnation. Seriously, if you are a devout catholic I suggest you leave this page and maybe read the Bible instead. In parthenogenesis an embryo develops from an unfertilised egg and the process occurs perfectly naturally in invertebrates like scorpions, and also in a select few vertebrates, like the Komodo Dragon (yes, it deserves capital letters). A normal egg cell produced by meiosis has the haploid number of chromosomes, as the other half of the offspring's genome is made up by the father's haploid sperm cell. However in parthenogenesis such haploid individuals are non-viable (may die during embryonic development or have a low zygote hybrid vigour) , and the parthenogenic offspring must often be diploid. Therefore full clones produced by parthenogenesis develop without the need for meiosis to manufacture haploid gametes in parents. But how is an embryo produced without without fertilisation? I hear you scream. Well, a mature egg cell is produced from mitotic oogenesis, which then develops directly into an embryo. This process is known as apomitic parthenogenesis, and is the less complex branch of the phenomenon. When parthenogenesis does occur with meiosis, offspring may be haploid, like the male ant, however there is often a complicated chain of processes which occur to restore diploidy to the offspring, in order to make them viable. However these offspring are only half clones of the parent organism, so they are genetically in-identical. But what I really want to talk about are the facultatively parthenogenic Komodo Dragons, which usually reproduce sexually, but can occasionally reproduce asexually. Therefore, when no viable males are present in a habitat, a female can ensure the survival of the species via parthenogenesis, making them more resistant to extinction than most species. What I particularly like about the Komodo Dragon, apart from its totally awesome name, is its ZW-sex determination, in which ZZ genotypes create males, ZW creates females, and in rare cases the WW genotype creates a female, however it is mostly unviable. Komodo Dragons are just too awesome for the XY sex determination system, although that may be a rather subjective analysis. In conclusion, the fact that an intelligent organism can clone itself in a pinch, to ensure the continued evolution of its species, is an incredible feat of mother nature. Imagine if we could induce parthenogenesis in humans? I mean, we've done it in fish...Actually, I don't like what I'm imagining. Bye!

Is this the Matrix?

Have you ever had a sudden panicked moment when you believe you've experienced something before? A conversation, a person or anything really. I know I certainly have, but thanks to science, I'm pretty sure that we are not all living in a computer generated world whilst robots harvest our body heat for energy. Deja Vu is not a glitch in the Matrix. The simplest, memory based, definition of Deja Vu is that a stimulus that triggers the feeling is linked to a similar memory that is already stored within the hippocampus, but which the person cannot remember. So if an event in the present has strong associations to a forgotten event in the past, then the feeling of Deja Vu is triggered. In 1941 researchers attempted to recreate the feeling in a laboratory, using hypnosis to induce post-hypnotic amnesia on volunteers. They were then shown a stimulus they had encountered before the hypnosis, yet only 3/10 people experienced Deja Vu. Spooky right? Although this test is of limited reliability given it's small sample size... so I wouldn't trust it implicitly. Recent virtual reality studies indicate that Deja Vu is more often triggered by the degree of familiarity felt in a certain situation, and so when a similar, familiar situation is encountered again, a person believes they have already lived through it. Location also appears to be important in this effect, as the degree of similarity between the spatial layouts of the previously experienced scene (which the person has forgotten) and the present scene increased the instance of Deja Vu in the VR test subjects. Cryptomnesia is another possible explanation for the phenomenon. I would like to take this moment to apologise to my readers who look down in haughty derision at the social sciences. Whilst I often do that myself, I thought this was too interesting a concept to pass up. Anyway brace yourselves, more unsupported conjecture coming your way. Cryptomnesia is essentially when information learnt is 'forgotten', but is still stored somewhere in the depths of the hippocampus, and is vaguely recalled based on more established concepts. The original memory is therefore distorted, and parts are omitted entirely. When this 'butchered' memory matches a current situation, Deja Vu is triggered. Each time we recall that 'memory' we are recalling our last construction of it. Deja Vu could therefore be a means of reconstructing and repurposing forgotten information to suit current needs. Although that theory does sound rather frivolous given its lack of scientific grounding. In truth, we don't fully understand the human brain, and researchers aren't really sure why Deja Vu like events are so different from person to person. Personally I think social conditioning has a part to play, as the populous are so aware of the phenomenon that they assume every half formed memory is Deja Vu. But then again, who doesn't want a little supernatural in their life?

Hibernate or hibernot

If the Land Rover advertising campaign is to be believed, us humans should not hibernate, as it is a waste of time during the cold winter months. Although, after reading new research published on the virtues of hibernation for neurodegenerative disorders, I believe this is an ill advised message. Who hasn't considered the concept of hibernation for humans? Just me? Ok, at first glance it doesn't seem a particularly attractive concept, going into a self induced 'coma-like' state during periods of low temperature, in a state of metabolic depression. Interestingly a process called  heterothermy occurs in hibernating mammals, during which they transition from being homeostatic endothermic to being ectothermic organisms, relying on their environment to regulate body heat, allowing for the slowing down of metabolic processes. The more you know right? But let's get back to the crux of this post: does hibernation actually have health benefits? Oh I'm so glad you asked. A UK team from the MRC Toxicology unit in Leicester have discovered the so called 'cold-shock chemicals' that cause mammals to destroy connections in their brains as they enter hibernation. Around 30% of synapses in the brain are destroyed, due to the slower metabolic rate during the winter. But what's truly amazing is that these culled synapses are reformed when the animal awakens in the spring! This obviously has huge implications for the medical profession, because the chemical released in the neural tissue as the animal begins to wake up and needs to repair synapses, RBM3, could be used to treat previously incurable conditions caused by prions, like Creutzfeldt–Jakob disease in humans. By artificially boosting levels of RBM3 in the brain, researchers have found that neurone death due to the misfolding of proteins caused by prions can be significantly reduced, and so we are one step closer to a drug that specifically targets the deadly neurone destroying agents that are prions. Memories are even retained after hibernation, as only the impulse receiving end of the synapses are destroyed (this is pretty obvious if you think about it, as a survival mechanism that wipes the animal's memory clean would be quite detrimental to its survival chances), and there is therefore a strong chance the RBM3 could be tailored into a drug to treat Alzheimer's patients, to slow down or even stop neurone loss during the early stages of the disease. Unfortunately the human body is not adapted to hibernate, as we don't produce enough RBM3 naturally, but I would certainly hibernate if given the chance. You would miss the most depressing months of the year, and reduce the risk of neurodegenerative disorders in later life. Stuff that in your gas-guzzling V8s Land Rover.

The MHCs: the immunological proteins you probably haven't heard of.

When one thinks of immunological proteins, you think of the big players; histamines, cytokines, and B/T cell receptors like CD4. However there are a little known family of proteins, that do play a vital role in the immune response, more specifically in antigen presentation, which make a bold claim in their name; the Major Histocompatability Complexes. In antigen presentation, a phagocyte like a macrophage or dendritic cell displays the antigens, which are specific peptide sequences used by the immune system to identify a pathogen, from the microbe it has just hydrolysed on its cell membrane. The protein the phagocytes use to do this is the MHC II. The phagocyte presenting these antigens will then travel to a lymphoid organ, the thymus or yellow bone marrow for example, through lymph and activate naive T cells. The CD4 receptor on the T cells must be able to dock to the MHC class II protein, so the epitope; the antigenic determinant which is recognised by the immune system, can imprint on the T cell receptor, priming it and therefore forming the effector T cells: the cytokine releasing T helpers which serve to rally the immune response, or the cytotoxic T killers which kill virally infected cells like homicidal spear wielding warriors. This in fact leads me on to the other class of Major Histocompatability Complex: MHC I. I made a passing reference to it as a 'surface marker' used in the immune response during a previous post, most people would stop there and move on to more significant proteins like interferon, but I'm not like most people (hence this blog). MHC I can be expressed on the surface membrane of almost every body cell, and it also displays the epitopes of antigens when, but for an altogether more sinister purpose... Ok that was slightly dramatic, but I doubt most people will read this far into the entry, so I can do what I want down here (whilst still remaining factually correct of course). The cells displaying epitopes on MHC I are virally infected, and can dock with the CD8 glycoprotein and the TCR found on the surface of T killer cells, and so they release cytotoxins like perforin, which destroys the cell membrane thus promoting PCD by apoptosis. How neat. So without this often overlooked protein, there would be no antigen presentation to trigger the adaptive Immune system, or pleasingly efficient destruction of virally infected cells. It just goes to show how interdependent every molecule in our bodies are, a principle that one should both admire and be absolutely petrified about...

Toxoplasma gondii: the parasite with a penchant for felids

If you hadn't already realised, dear readers, I'm a huge nerd. Wipe that look of shock off your faces. Anyway, I've been extremely busy with Pokemon Alpha Sapphire, revision and Fullmetal Alchemist. I'm only human ok! I've also been working tirelessly on my Extended Project, a 5,000 word dissertation of the topic of feline intelligence. Most people chose sensible topics like stem cell research, the UK's involvement in the EU, or the parallels between historical leaders, but I, in an attempt to make my life that little bit more difficult, decided to pick a topic that has very little debate, and even fewer people who are interested in the answer. Whilst I was researching the controversial topic of the intelligence of the domestic cat, I stumbled upon a parasite known as Toxoplasma gondii (T. gondii), as T. gondii's primary host is the domestic cat. T. gondii is a unicellular eukaryotic organism, a protozoan, that causes a disease called Toxoplasmosis in human host cells. Toxoplasmosis is the root of the term 'crazy cat lady' syndrome, as there is a definite link between the disease and mental health issues like schizophrenia, although most hosts are just symptomless carriers. Great. That's what I've got to look forward to.  It is one of the most common parasites found in the human body, and it is estimated that 1/3 of the global population is infected. The parasite can reproduce asexually within virtually all exothermic mammals, however it can only reproduce sexually in the intestines of Felids. This basically means it can only adapt and change its structure to evade our immune systems within cats, making them its definitive host. In order to optimise its chances of infecting cats, T. gondii can alter the behaviour of intermediate hosts like mice, to make them attracted to the scent of cat urine, so they are more likely to be preyed on by a passing feline. To do this the parasite hijacks white blood cells, which seem to be the target for pathogenic attack quite frequently (even parasites have a sense of humour). The WBCs are converted into chemical factories, synthesising neurotransmitters like serotonin, to reduce response of fear and anxiety that usually occurs in the amygdala of the mouse, as soon as it smells a feline nearby. The parasite resides within a membrane known as an oocyst until it passes through the stomach and the membrane is hydrolysed. It then infects epithelial cells, in which it is converted to Tachyzoite cells, speeding up the rate of proliferation, then they are converted to slow dividing Bradyzoites, which form tissue cysts in the host, completing the parasite's lifecycle. It's a feat of biological adaptation that a parasite can become so ultra-specialised to one particular host, but like a lot of evolution and natural selection, this mechanism is kept because it works. It worked during the evolution of the parasite, and so that's what it does to this day, and what it will continue to do until domestic cats develop a resistance to it. T. gondii stubbornly resists change, and that's why I like it...

Vitamin D: the mechanism, the molecule, the screenplay

What's hip loyal biologists? (obviously not this blog) Today on my quest for knowledge of our biological universe, I came across the fascinating, fat soluble steroid known as Vitamin D. The D2 and D3 molecules to be more precise. You've probably heard of rickets, and a bit about how the sun stimulates Vitamin D's release in our bodies. If you're an introvert obsessed with science and video games like me, then you know where I'm coming from. Vitamin D is vital in our bodies to enhance absorption of key minerals in the intestinal system, like calcium, iron or zinc. These elements are used to construct and maintain our skeletal system, so that's why if children develop a vitamin D deficiency, their bones can become elongated and deformed, because they cannot absorb enough calcium or phosphorous for proper skeletal development. Although this mostly occurs in countries with a high prevalence of genetic disorders such as pseudovitamin D deficiency rickets. Vitamin D is marketed on the internet as a miracle cure for conditions like cancer, heart disease, depression and autoimmune disease, despite the fact that no clinical trials have proven this claim. In fact they mostly say Vitamin D has a negligible impact on such conditions. The D3 vitamin molecule is produced in the skin, when exposed to UV light, from another molecule called 7-dehydrocholesterol. This precursor of vitamin D3 is produced in relatively large quantities, in fact 10,000 to 20,000 IU of vitamin D are produced in 30 minutes of whole-body exposure, in the skin of most vertebrate animals. 7-dehydrocholesterol is converted into D3 by UVB rays between 270 and 300 nm, but occasionally an equilibrium can form in the skin, in which vitamin D degrades as fast as it is synthesised. But that's not the end of vitamin D's journey in the body. In the liver it is converted into a prohormone (precursor to a hormone) known as calcidiol, and then it is converted yet again in the kidneys, but this time to its biologically active form; calcitriol (a bit like phytochromes in plants for you botanists out there) . Calcitriol binds to the vitamin D-binding protein, which transports it to vitamin D-rerceptors (VDRs) on the surface of target cells. Here's where it gets really good. The VDRs bound to vitamin D will act as transcription factors, promoting expression of transport proteins like TRPV6 (catchy right?) within cells,  which are involved in absorption of calcium in the immune system. So what have we learnt? For one thing the proteins and receptors involved with Vitamin D have incredibly uncreative names. But on a more serious note, sunlight is essential to skeletal health, so maybe we should embark on adventures is the great outdoors more frequently! I'm such a hypocrite... 

Avian flu: taking flight?

On 16th November a duck breeding farm in Yorkshire tested positive for avian flu, so as you can imagine DEFRA was on the scene immediately, introducing a 10km restriction zone and culling all 6,000 birds on the farm to prevent further spread of the disease. But why? Is avian flu so contagious, that such an extreme response was warranted? Is it that dangerous? Let's find out shall we. Avian flu is caused by the influenza A strain of the influenza virus (although A does not stand for avian). All subtypes of influenza A are adapted to be able to use birds as a host, but are not always zoonotic (can pass from animals to humans). Influenza A is what is known as an  single stranded antisense RNA virus, meaning its single strand of RNA (3'-5') runs complementary to viral mRNA (5'-3')  that it encodes. This means it must carry RNA polymerase within the virion particle, as the viral RNA cannot be directly translated into protein, it  must be transcribed first, rather like DNA. Influenza A can be categorised into 2 subtypes based on the protein used to construct its membrane: Hemagglutinin (H) or Neuraminidase (N) . The H protein causes agglutination of red blood cells in the host, and mediates the binding of a virion particle to the host cell and entry of the viral genome into the host cell genome.  Whereas N is an enzyme that breaks the glycosidic bonds in the monosaccharide, neuraminic acid, commonly found in animal cells as glycoprotein and it also controls the release of new virion particles from host cells. Different strains of influenza virus encode for different types of N and H which all play a specific role in the viral lifecycle, for example H5N1 virus  contains type 5 Hemagglutinin and type 1 Neuraminidase (oh how I love arbitrary numbers used to name pathogens). Interestingly, these 2 proteins form the antigens that allow antibodies produced by B cells to bind to the microbe, so macrophages can phagocytose it. Ok,  I think I've indulged you enough in the virus' structure and nomenclature, so let's talk about the birds. The outbreak in Yorkshire recently was H5N8 strain, which is of very little threat to people. In fact no one has died from it. Ever. The avian flu strains that you really have to worry about are H7N9 continually reported in poultry in China, and H5N1, which has a 60% case mortality rate across 15 countries (since 2003). Migratory fowl can act as asymptomatic carriers for the virus, which is probably how it reached the UK in the first place, and strains like H5N1 are not limited to birds and people; in New England 400 harbour seals were killed by the pathogen in a 1978 epidemic. Ok, so we know that certain strains of influenza A are deadly to people, but if the H5N8 strain poses no threat to us, why were all the ducks killed? Well, because of the high mutation rate of the virus, and its ability to hybridise with strains from other species, it could quickly become a human epidemic. So before we start arguing over the 'poor ducks' that were 'murdered', we must consider the potential threat of any strain of influenza to humans.