Horizontal Gene Transfer: How parasites control insect host behavior

Published recently in the journal Current Biology, research from a study conducted by the RIKEN Center for Biosystems Dynamic Research has revealed that parasites likely manipulate the behavior of their host organisms using horizontal gene transfer. 

In general, many parasites control their hosts to ensure the survival and reproduction of their species. One example of such a parasitic species is the horsehair worm, born in water but migrating to dry land using aquatic insects. After being eaten by a mantis (terrestrial insect), the worm grows within the host, beginning to manipulate its behavior. Once fully matured, the horsehair worm prompts the insect host to jump into the water and drown to its death, allowing the parasite to complete its life cycle and reproduce. 

Interestingly, previous studies have indicated that the horsehair worm likely manipulates the host’s biological pathways to increase movement towards the light (and approach water) by mimicking molecules found in the hosts’ central nervous system. To better understand how they developed such a mimicry mechanism, researchers analyzed the whole-body gene expression in a Chordodes horsehair worm before, during, and after host manipulation. From this study, researchers found over 3,000 genes that were expressed more during manipulation and 1,500 that were expressed less. In contrast, gene expression in the mantis brain did not change whatsoever, indicating that the parasites were producing proteins that would manipulate the host nervous system. After further analysis, interestingly, it was found that over 1,400 hairworm genes that matched those found in their mantis hosts were absent in species with different hosts. From these findings, researchers concluded that the identified mimicry genes (linked with neuromodulation, light attraction, and circadian rhythms) were likely the results of multiple horizontal gene-transfer events from various mantis species during the evolution of horsehair worm species.

Considering that horizontal gene transfer is far more common in prokaryotes, it was rather interesting to see an application of this phenomenon in eukaryotic species. This was especially the case since it is a primary way through which bacteria evolve antibiotic resistance. In that sense, horsehair worms would likely make ideal model organisms to study the mechanism by which horizontal gene transfer occurs and allows molecular mimicry, advancing current scientific understanding of evolutionary adaptation.

Click here to view the ScienceDaily article release

Click here for more information regarding this research study

A Breakthrough in Gene Activation

Recent research performed at New York University has shed a little bit of light on exactly how certain proteins know when to activate genes. Prior to this experiment, we knew that there were proteins responsible for activating and deactivating different genes, but the conditions necessary for the proteins to do so. This experiment has determined a new, previously unknown, set of rules that cells use in activating genes under certain conditions by working with Drosophila. By manipulating the Zelda protein in fruit flies, which is responsible enhancing the ability of the Dorsal protein that codes for embryonic nervous system development in Drosophila, the researchers were able to see under what conditions the enhancement of this protein impaired or improved nervous system development. Mutating the Zelda binding sites resulted in a change in the onset of activation, the activation severity, and the overall rate of activation. This led the scientists to isolating the Zelda protein, and they came away with the observation that the cell made decisions in regards to the expression and activation of the gene responsible for neurological development.

I find this work very fascinating. The mechanism behind the experiment can be a little bit confusing, but the significance of the work cannot be denied. Because the mechanism behind the genes in Drosophila are similar to that of humans, the ability to know how our genes are activated and what factors affect the activation of certain genes will prove to be incredibly useful moving forward, particularly in the treatment of diseases. For example, if a disease results in an undeveloped brain or nervous system, this information could allow doctors to increase activation of a certain gene within the embryo, if future science makes this possible. Even if this does not become possible, gaining a better understanding on how gene expression works in general is an impressive breakthrough and worth knowing moving forward.

Regenerative Nerve Connection in Lampreys

An article by the University of Missouri-Columbia describes why lampreys, an eel-like organism, is important to neurobiology studies. A lamprey has a simple nervous system with the ability to regenerate nerve connections and recover normal mobility within eight weeks of a spinal cord injury. The first genome for the species was recently completed. A new study led by neurobiologists David Schulz and Andrew McClellan annotates the sequences of 47 ion channels across the genome. The scientists "used bioinformatic tools to identify sequences from the lamprey genome that could potentially belong to ion channel families and then performed phylogenetic and gene expression analyses across nervous system tissues to confirm the identifications". Ion channels are pores in the cell membrane that transport ions. There are significant because in nerve cells, they are crucial for transmission and processing electrical signals. Researches believe knowing these sequences will provide for more rigorous study of the nervous system.

I think the study is beneficial because it can give researches a detailed picture of ion channels in the nervous system. They will be able to understand the structures and their individual functions better. They also can target specific gene sequences and see how they can modify their expression. 

A Genetic Oddity May Give Octopuses and Squids Their Smarts

According to a study from NY times, Coleoid cephalopods are the most intelligent invertebrates for their behavioral complexity through RNA editing. Coleoid cephalopods is a group compassing octopus, squids, and cuttlefish. Research has revealed that natural selection favored the RNA editing of the coleoids and slowed the DNA-based evolution that helped the organisms to have beneficial adaptations over time. The enzymes of these cephalopods swap out some of the letters (ACGU) of RNA encoding and produced modified RNA which creates proteins that weren't originally encoded in the DNA sequences. The coleoid genes share tens of thousands of these RNA editing sites which markably contained DNA mutations that leads to the source of new traits for adaptation of the organisms. Additionally, the RNA editing allows the invertebrates to swiftly manipulate their nervous system and to have dynamic control over proteins based on different environmental conditions or tasks. In octopus, RNA editing aids to quickly adapt to the changes in temperature.

I find it very interesting how the swapping of the RNA encoding letters in the coleoid genes creates DNA mutations which leads to advantageous traits for the organisms for adaptation. It is amazing how mutations in these invertebrates can be beneficial while in humans it can cause major defects.

A small molecule in animals that was thought to have no impact is now thought to control precise movements in animals

Scientists at the University of Sussex working with fruit flies have found that the flies could not flip themselves upright after being placed upside down when changes were done to its miRNAs. MiRNAs affect the formation of the nervous system, but may now also be linked to controlling specific movements. Researchers originally tried switching off individual microRNA molecules to investigate the effects it had on the nervous system when they found out that flies could not sit themselves upright after being placed upside down. Scientists are now wondering what different miRNAs affect different movements. Scientists hope to use this information to understand how nervous system disorders lead to the loss of movement in humans.

This article is interesting because the scientists were testing the nervous system and accidentally found out that  molecules encoded in the genome of all animals can have an affect on movement which was otherwise unknown.  Hopefully scientists in the near future can learn more about what miRNA molecules controls what which can lead to a better understanding of nervous system disorders and how to fix or treat them. 

You can find the original article here.

Ctenophore Genome Sparks the Theory that the Neuron has Evolved Twice

Recent research in neuroscience and genetics has led to the idea that the neuron, previously thought to have only evolved once, has gone through two separate spurts of evolution. By examining the genome and neuromuscular structure of ctenophores, researchers are finding that the nervous system and immune system of this clade of animals has come around almost entirely independent from other animal groups - from the closely related proiferans to our own bilaterian grouping. The researchers examined the genomes of two model ctenophores, Pacific sea gooseberries and comb jellies (pictured above), to examine how these species expressed genes involved in their muscular system, nervous system, and immune system. The researchers used the genomes to place ctenophores at the base of the phylogenetic tree (pictured below), adding to the idea that ctenophores likely evolved separately from the rest of animal phylogeny. The examination of the immune system genetics found that the ctenophore immune system differs greatly from bilaterians, sponges, and cnidarians, lacking rather important pattern recognition markers. Genes involved in body patterns and axis formations were also found lacking in the ctenophores, despite being present in all metazoans. The examination of the nervous system of ctenophores found that ctenophores use practically none of the neurotransmitters known to be used in cnidarians and bilaterians (i.e. serotonin, adrenaline, dopamine, glycine, acetylcholine), suggesting these neurotransmitters are adaptations of the later cnidarian and bilaterian lines. While there are some neuron-related genes in the ctenophore that are shared by bilaterians, the neurons of the ctenophore do not express these shared genes. The similarity between ctenophores and later metazoans along with the stark differences in the nervous, muscular, and immune system as well as the genetic identification of ctenophores as a basal group supports the idea that ctenophores evolved independent from and parallel to the later metazoans. 

In easier terms, the findings of this research give way to the idea that the ctenophore phylum evolved separately from other phylums. This contrast previous ideas of ctenophores as an ancestor to later species and groups. This finding is especially interesting in the scope of neuroscience, as the previous way of thinking had the ctenophore nervous system as an ancestral system for later species, including bilateria. This research leads us to believe that, instead of a single, continual development of the nervous system, the nervous system instead evolved in two separate events - that of the ctenophore and that of the following phylums. This researching finding means that there are two entirely separate organizations of the nervous system that have evolved entirely independent of each other. Looking at nervous system evolution through this light means that the origin and evolution of our own nervous system is not as clear as we had once thought.

(second phylogeny image source: https://whyevolutionistrue.wordpress.com/2013/12/20/the-outgroup-for-animals-ctenophores/) 

Cold-Induced Pain Linked to the Garlic, Mustard Receptor

Depicted Above: Researchers Edward Högestätt, Lavanya Moparthi, Urban Johanson and Peter Zygmunt.

A group of researchers from Lund University in Sweden identified what causes the connection between cold and pain. Ten years ago they discovered the receptor that reacts to the substances in mustard and garlic. The purpose of this experiment was to see if this receptor also responds to cold, which seems to be the case. 

The research group's findings "increase our knowledge of the human body's temperature senses, [and can] also help all those who suffer from cold allodynia [: people] who are over-sensitive to cold and experience pain when exposed to cold." Edward Högestätt explained how these issues occur in patients containing chronic pain or diseases that affect the nervous system, like diabetic neropathy. "Patients undergoing chemotherapy can also become over-sensitive to cold as a side-effect of their medication. The discomfort and pain experienced by patients can start at relatively mild temperatures, within the temperature span to which the mustard and garlic receptor reacts." Peter Zygmunt states that we now know the mustard and garlic receptor reacts to temperatures under 20°C, thanks to this experiment. Additionally, the chilli receptor reacts to temperatures over 42°C (burning your hand), while the menthol receptor reacts to temperatures under 28°C (pleasantly cooling).

The research group believes that if the receptors that cause pain from cold temperatures are blocked, than pain will be relieved for individuals undergoing this issue. Because of this, drugs designed to block the receptors that cause itching, incontinence and pain are in the midst of being created. Potential new drugs for people who are affected by perfume, solvents, cigarette smoke, car exhausts can also benefit those who are over-sensitive to cold in the airways, since the mustard and garlic receptors are sensitive to this. I think this is very convenient for individuals who suffer from these conditions. New drugs that help people sensitive to these conditions can relieve a lot of stress and other issues that arise from these sensitivities. However, the expense for these drugs may not be worthy for individuals who cannot afford them, or even feel they are necessary. Pharmaceutical companies should definitely take this concept into consideration.

Article:
http://www.sciencedaily.com/releases/2014/11/141113085154.htm

Related Article: 

http://www.news-medical.net/news/2006/03/28/16936.aspx

Genetic discovery from UCL Institute of Child Health and Great Ormond Street Hospital could lead to neurodegeneration treatments

     A team from the UCL Institute of Child Health and Great Ormond Street Hospital could be on the verge of developing new therapies to handle neurological degeneration and loss of motor skills. After reading an article in the American Journal of Human Genetics, the team led to identify a rare condition that causes poor motor control and intellectual disability. It was found that an absent protein that causes the syndrome could be the key to find new and improved treatments.

     Two teams, ICH researches and GOSH clinical geneticists worked together and identified specific characteristics in two unrelated families. The affected children had moderate to severe intellectual disability, progressively coarsening facial features and limited hearing and speech. The children also had relatively large heads. Even though their heads were quite large, they had a relatively small cerebellum. Having a small cerebellum could be damaging due to the fact that it is the part of the brain normally packed with neurons, which play a key role in controlling motor function. As stated in the article, “all the children had limited mobility as a result of this cerebellar atrophy; four could only walk with assistance, and two had not progressed beyond crawling.”

     To discover a mutated gene found in both families, the teams used genetic mapping and next generation sequencing. The findings determined the syndromes that the children had were due to the mutation. The mutation of the affected gene, Sorting Nexin 14 (SNX14), led to the loss of a protein that is crucial to development. Because the researchers were able to identify the absent protein, they hope to develop new drug therapies to help development continue without the mutation affecting it.

     The team is hoping to continue the research with those missing the protein to help find a cure. As said by the team, "We can now develop model systems to help us in this task and potentially develop therapeutic treatments that might prevent or alleviate neurodegenerative damage, which leads to loss of both motor and intellectual function."

     Finding that the absence of a specific protein in the cause of this syndrome is remarkable. Knowing the cause is the first big step. Finding the drug or therapies to cure or treat this will be a lot easier now that scientists have a specific area to target.


Article: http://www.medicalnewstoday.com/releases/285018.php

Pigs, Fish, and Jellyfish are Being Used to Trace Nervous Disorders in Humans

A recent article explains how scientists at Aarhus University are using pigs, jellyfish, and zebrafish as a tool in identifying and understanding hereditary forms of diseases that affect the nervous system. Specifically, disorders such as Parkinson’s disease, Alzheimer’s disease, epilepsy, and forms of ALS are being studied. In pigs, scientists have focused on the SYN1 gene, which encodes for the protein that is involved in communication between nerve cells, synapsin. Synapsin occurs primarily in the nerve cells of the brain, so parts of the SYN1 gene are capable of being used to control the expression of genes that are connected to hereditary versions of various nervous disorders. In order to ensure that the SYN1 gene was exclusively expressed in nerve cells, scientists attached the gene to the green fluorescent protein gene in jellyfish and put it into zebrafish. Senior scientist Knud Larson of Aarhus University explained why GFP was attached to the SYN1 gene: "We could clearly see that the transparent zebrafish shone green in its nervous system as a result of the SYN1 gene from humans initiating processes in the nervous system. We could thus conclude that SYN1 works specifically in nerve cells.” 

Disorders of the nervous system typically involve some loss of cognitive or physical function

The SYN1 gene was then inserted into pigs, mainly because the animal is incredibly well suited as a model for human diseases. Pigs are specifically being used to study nuerodegenerative diseases, such as Parkinson’s disease. In addition to studying nervous disorders through controlling the expression of the SYN1 gene, the gene may also be used in the future for research pertaining to fetal development of the brain and nervous system. I chose this article because I believe that it is truly incredible that these diseases which affect the nervous system are being studied more in depth. Many of these disease are incurable and terminal, so many studies pertaining to such diseases have only been performed after an individual or subject has died. Targeting the gene that controls the expression of synapsin can definitely lead to better treatment for disorders of the nervous system. If scientists can control the expression of the SYN1 gene in order to create disease in test subjects, then it is not radical to think that the expression of the gene can then be used to reverse the symptoms of such nervous disorders. 

Pigs are used because they are readily available and they closely mimic humans in their relative size, genetics, and their anatomy and physiology

Inheritance of various nervous disorders

Mouth-watering Artifical Glands

  It is proven that glands that make tears and saliva can be bio engineered to take on the function of a normal gland, when they were tested on mice.  Tsuji of the Tokyo University of Science collected cells that would have turned into tear and salivary glands from mice embryos and grew them for 3 days in devices that mimicked conditions of a developing embryo. 

  The glands were then transplanted into the mice the natural glands were taken from.  Once transplanted, the tissue matured then eventually connected with the mouse's nervous system and tear and saliva ducts.  The glands and ducts produced fluids when given the correct stimuli.  It's amazing how science can do so many things nowadays and has little restrictions.  If a person has a deformed duct or gland I'm guessing that they can fix it by transplanting a new one.  Science has come a long way from what they were limited to in the past, I think they are only going to advance even more.


http://www.medicalnewstoday.com/articles/266952.php
http://www.thenews.com.pk/article-120729-In-lab-dish,-scientists-make-tear-and-saliva-glands

A new way to study nervous system cell death

In this article Michael Lehmann a professor in biological science finds a new way to understand cell death in the nervous system. They use fruit flies to find the nmda receptor, which triggers cell death. This is important for today to help understand the affects of nerve diseases. This article is important since today you hear about Alzheimer’s and diseases like that.  It also shows the cell death in the human immune system which can help understand hiv and aids.  In order to study cell death researchers ar using salivary glands in fruit flies larvae.  Brandy Ree who has worked with Lehmann in an attempt to define the pathway that leads from activation of the receptor to the cell's eventual death.  There will be further studies as the group was granted a three year 260,000 dollar grant.  I looked up cells of the nervous system and learned a lot about each cell and what its function is so I thought I would share it.



article: http://www.sciencedaily.com/releases/2013/04/130403121943.htm

other article: http://www.albany.edu/faculty/cafrye/apsy601/Ch.02cellsofthenervoussystem.html

A Shrinking Brain

A little boy named Jason Egan from Australia has a condition that is possibly a new mutation never before recorded in history. Since he was about two years old, he was diagnosed with Cerebral Palsy because of his tense muscles, and his speech- but when he was 6 years old everything changed. Jason had learned sign language to communicate, and could even say a few words, but he seemed to start rapidly deteriorating. He could no longer sign, speak, or even feel pain. Doctors began testing him for every neurological condition under the sun, and one scan showed that his brain was actually shrinking.

[caption id="" align="alignleft" width="208" caption="Jason Egan, with His Father"][/caption]

The news of the child's shrinking brain baffled doctors, and since this discovery he has negatively tested for every known neurological disorder that there is. It is thought that Jason has a unique mutation that has caused his brain to shrink, most notably the Cerebellum, the part of the brain that controls movement. The good news, however, is that Jason's brain has stopped shrinking as a recent brain scan showed. The overall size of his brain has not changed and doctors indicate that this is a good sign, and he may be able to live a life similar to that of a person with cerebral palsy. While this situation is a depressing one, it opens new doors in the fields of genetics and neurological dis0rders.