From traditional medicine to personalized medicine

From prehistory, where medicine started began with plants, minerals and parts of animals; until today, medicine has evolved very quickly. Much of the “fault” of his fact is due to genetics, which allows us to talk about personalized medicine. In the following article we discuss this.

THE EVOLUTION OF DISEASES

To talk about medicine, we have first to know diseases. We cannot think that all diseases are genetic, but there are diseases related to anatomical changes, fruit of our evolution.

Chimpanzees are the closest animal to us, humans, with which we share 99% of our genome. Despite this, humans have very particular phenotypic characteristics as the brain most develop, both in size and expansion of the cerebral cortex; hairless sweaty skin, bipedal posture and prolonged dependence on offspring, allowing the transmission of knowledge for longer; among other.

Possibly, the bipedal position was key to the early development of the divergence between the chimpanzee lineage and that of humans; and is also the reason for the appearance of some diseases related to anatomical factors. Among them are hernias, haemorrhoids, varices, disorders of the spine, such as herniated intervertebral discs; osteoarthritis in the knee joint, uterine prolapse and difficulties in childbirth.

The fact that the pelvis was remodelled (Figure 1) and narrower resulted in obstetric problems millions of years later, when the brain expanded. Consequently, the skull as well. The heads of the foetuses were longer and larger, making birth difficult. This explains why the deliveries of humans are longer and longer compared to those of chimpanzees and other animals.

Figure 1. Comparison between human pelvis and chimpanzee pelvis in bipedal position (Source: Libros maravillosos – La especie elegida (capítulo 5))

The evolution towards modern life has behaved many changes in every way. In comparison to our hunter-gatherer ancestors (Figure 2), our diet has changed a lot and has nothing to do with what other primates eat. For the latter, the fruit represents most of the intake, but for us it is red meat. In addition, we are the only animals that continue to feed us milk after the lactation period.

Figure 2. Picture of hunter-gatherer humans (Source: Río Verde en la historia

If we add to the sedentary lifestyle and the limited physical activity of modern humans, it can help explain the seriousness and frequency of some modern human diseases.

Lifestyle can also affect us. For example, myopia, which rate is higher in western individuals who read a lot or do activities of near vision, compared to individuals of Aboriginal’s towns.

Another clear example is the alteration in the female reproductive stage. Currently, women have children more and more later. This is also linked to a decrease in the duration of breastfeeding. These changes, which can be considered socially positive, have negative effects on the health of the reproductive organs. It has been shown that the combination of early menarche, limited or no breastfeeding and later menopause are the main risk factors for breast and ovarian cancer.

Humans increasingly live more years and we want the best quality of life. It is easy for more longevity to appear more diseases, by the deterioration of the organism and its cells.

THE EVOLUTION OF MEDICINE

The history of medicine is the history of the struggle of men against disease and since the beginning of this century, is also the history of human effort to maintain health.

We have acquired the scientific knowledge of medicine based on observation and experience, but it has not always been so. Our ancestors experienced sickness and the fear of death before a rational picture could be made of them, and the medicine of that time was immersed in a system of beliefs, myths and rites.

However, in the last years it has been born personalized genomics, which tells you your risk factors. This opens a door to personalized medicine, which adjusts treatments to patients depending on their genome (Figure 3). It uses information from a person’s genes and proteins to prevent, diagnose and treat a disease, all thanks to the sequencing of the human genome.

Figure 3. Personalized medicine that treats people individually, according to their genome (Source: Indiana Institute of Personalized Medicine)

Molecular methods that make precision medicine possible include tests of gene variation, proteins, and new treatments targeting molecular mechanisms. With the results of these tests and treatments can determine the state of the disease, predict the future state of the disease, the response to the drug and treatment or even the role of the food we eat at certain times, which results of great help to the doctors to individualize the treatment of each patient.

To do this, we have within our reach the nutrigenetics and the nutrigenomics, that like the pharmacogenetics and the pharmacogenomics, they help the advance of a medicine is more and more directed. Therefore, these disciplines are today one of the pillars of personalized medicine since it involves treating each patient individually and tailor-made.

The evolution towards precision medicine is personalized, preventive, predictive and participatory. There is increasing access to information and the patient is more proactive, getting ahead of problems, preventing them or being prepared to deal with them efficiently.

REFERENCES

• Varki, A. Nothing in medicine makes sense, except in the light of evolution. J Mol Med (2012) 90:481–494
• Nesse, R. and Williams, C. Evolution and the origins of disease. Sci Am. (1998) 279(5):86-93
• Mackenbach, J. The origins of human disease: a short story on “where diseases come from”. J Epidemiol Community Health. (2006) 60(1): 81–86
• Main picture: Todos Somos Uno

Sequencing the human genome

Genomics is a new science which has had a very important boom in recent years, thanks to advanced technologies of DNA sequencing, advances in bioinformatics and increasingly sophisticated techniques for analysing whole genomes. And I will discuss in this article about whole genomes and their sequencing, mentioning the Human Genome Project, which allowed the sequencing of the human genome.

WHY WE SEQUENCED?

Sequencing is the set of methods and biochemical techniques aimed at determining the order of nucleotides (A, T, C and G). Its objective is to get in order all nucleotides DNA of an organism.

The first organisms sequenced were two bacteria, Haemophilus influenzae and Mycoplasma genitalium in 1995. One year later, the genome of a fungus was sequenced (Saccharomyces cerevisiae).

From that moment comes the eukaryotic sequencing project: in 1998 Caenorhabditis elegans (nematode) was sequenced, in 2000 Drosophila melanogaster (fruit fly) and in 2001 the human genome.

But, why we sequenced? In the case of human genome, there is the need to know to help alleviate or prevent diseases.

Some of the organisms sequenced are model organisms, which have:

• Medical importance: there are pathogens and we know diseases that they can cause.
• Economic importance: organisms that humans eat, they can improve with the molecular techniques.
• Study of evolution: in 2007 more than 11 species of Drosophila were sequenced and it tried to understand the evolutionary relationship between their chromosomes. It has also been made in mammals (ENCORE Project).

WHAT WE UNDERSTAND FOR GENOME SEQUENCED?

The human genome has 46 chromosomes, it means 23 chromosome pairs (22 autosomal chromosome pairs and 1 sexual chromosome pair, XX or XY depending if it is female or male).

The size of the human genome sequenced is 32,000Mb, 23 chromosomes plus Y chromosome.

The human genome was obtained from the mixture of human genomes to obtain a representation of all humanity genome.

PARADOX THAT WE FIND IN GENOME

A paradox is a statement that, despite apparently sound reasoning from true premises, leads to a self-contradictory or a logically unacceptable conclusion. In genomes we find two clear paradoxes.

The first one refers to the C-value, which represents the amount of DNA in the genome. As would be expected, if the organism is larger and more complex, the size of its genome will be bigger. However this is not true because there is not this correlation. It is due because the genome not only contains coding genome and proteins, but also contains repetitive DNA. In addition, the most compacted genomes are found in organisms less complexes.

The second paradox refers to the G-value, which represents the number of genes. There is no correlation between the number of genes and its complexity. A clear example is that in human genome has around 20,000 genes and Arabidopsis thaliana (herbaceous plant) has 25,000 genes. The reason is found in the RNA world, which is more complex and it is related to gene regulation.

THE HUMAN GENOME PROJECT (HGP)

The human genome sequencing project has been the most important biomedical research project of the whole history. With a budget of 3 thousand millions of dollars and the participation of an International Public Consortium, which was formed by EEUU, UK, Japan, France, Germany, China and other countries. Its ultimate objective was achieving the complete sequence of the human genome.

It started in 1990, but things get complicated when, in 1999, appeared a private company, Celera Genomics, headed by the scientist Craig J. Venter, who launched the challenge of getting the human sequence in record time, before the expected by the Public Consortium.

At the end it was decided to leave in a draw. The Public Consortium accelerated the process and obtained the draft almost at the same time. On 26^th June 2000, in a ceremony at the White House with President Bill Clinton, the two leading representatives of the parties in competition, Craig Venter by Celera and the Public Consortium director, Francis Collins found. It announced the achievement of two drafts of the complete human genome sequence (Video 1). It was a historic moment, as the discovery of the double helix or the first time the man went to the Moon.

Video 1. Human Genome announcement at the White House (Source: YouTube)

The corresponding publications of both sequences did not appear until February 2001. The Public Consortium published its sequence in the journal Nature, while Celera did in Science (Figure 1). Three years later, in 2004, the Consortium published the final or complete version of the human genome.

Figure 1. Covers publications of the human genome sequence draft in Nature and Science magazines in February 2001 (Source: Bioinformática UAB)

PERSONAL GENOMES

The genome of the year 2001 is the reference genome. From here we have entered in the era of personal genomes, with names and surnames. Craig Venter was the first person who sequenced his genome, and the next one was James Watson, one of the discoverers of double helix.

It took 13 years to sequence the reference genome. It took less time to sequence Craig Venter’s genome and only few months for Watson’s genome.

CLINICAL APPLICATIONS OF SEQUENCING

Without going to sequence the entire genome they have been identified disease-causing genes. An exome is not the whole genome, but the part of the genome corresponding to exons.

An example is the case of Nicholas Volker (Figure 2), the first case of genomic medicine. This child had a severe and intractable inflammatory bowel disease of unknown cause. With exome sequencing was allowed to discover a mutation in the XIAP gene on chromosome X, replacing an amino acid functionally important for another. A bone marrow transplant saved the life of the patient.

Figure 2. Nicholas Volker with his book One in a Billion, which tells his story (Source: Rare & Undiagnosed Network)

REFERENCES

• L. Pray. Eukaryotic genome complexity. Nature Education 2008; 1(1):96
•  Brown. Genomes 3, 3rd edition (2007)
• Bioinformática UAB
• BT.com
• E. A. Worthey et al. Making a definitive diagnosis: Successful clinical application of whole exome sequencing in a child with intractable inflammatory bowel disease. Genetics in Medicine 2011; 13, 255-262

• Main picture: Noticias InterBusca

Hybrids and sperm thieves: amphibian kleptons

In biology a hybrid is the result of the reproduction of two parents of genetically different species, although in most cases hybrids are either unviable or sterile. Yet in some species of amphibians, sometimes hybrids are not only viable, but also become new species with special characteristics. In this entry we’ll show you two cases of amphibian hybrids that form what is known as a klepton and that make the definition of species a little less clear.

WHAT IS A KLEPTON?

A klepton (abbreviated kl.) is a species which requires another species to complete its reproductive cycle. The origin of the word klepton comes from the Greek word “kleptein” which means “to steal”, as the klepton “steals” from the other species to reproduce. In the case of amphibians, kleptons have originated from hybridation phenomena. The amphibian’s potent sexual pheromones and the multispecies choirs in the case of anurans, causes some males and females of different species to try to mate together. Yet hybrids are only viable between closely related species.

Among the different klepton species we can encounter two different methods depending on the type of conception: zygokleptons, in which there’s fusion between the egg and the sperm’s genetic material, and gynokleptons, in which the egg needs the stimulation from the sperm but doesn’t include its genetic material.

The different amphibian kleptons are usually constituted entirely by females (there are usually few or no males) that use the sperm of another species to perpetuate the klepton. As some kleptons depend on various related species, this can promote the creation of “species complexes” in which various similar species present hybridization areas and very complicated relationships among them. Below you’ll find two klepton examples, one in European anurans and the other in American urodeles.

HYBRIDOGENESIS IN WATER FROGS

The European water frogs (Pelophylax genus) form what is known as a “hybridogenetic complex” in which the hybrids from different species form kleptons which can’t reproduce among each other but, which must reproduce with a member of one of the parental species, “stealing” or “parasitizing” its sperm in order to survive.

Photo by Bartosz Cuber of two edible frogs (Pelophylax kl. esculentus) in amplexus. This is the best known hybrid both because of its wide distribution, and for being considered a delicacy in France.

In the hybridogenesis of water frogs the genetic material of both parents combines to form the resulting hybrid (zygoklepton). This hybrids (almost always females) will have half their genome from one species and half from the other. Yet, not being able to reproduce with a similar hybrid, during gametogenesis the hybrids eliminate the genetic material from one of the parent species. This way, when reproducing with an individual from the species whose genetic material has been deleted, they will form another hybrid.

Scheme of the genetic composition of the different Pelophylax kleptons. In this hybridogenetic complex four “natural” species intervene: the marsh frog (Pelophylax ridibundus, RR genome), the pool frog (Pelophylax lessonae, LL genome), the Iberian waterfrog (Pelophylax perezi, PP genome)  and the Italian pool frog (Pelophylax bergeri, BB genome).

The edible frog (Pelophylax kl. esculentus, RL genome) comes from the hybridization between the marsh frog and the pool frog. The Italian edible frog (Pelophylax kl. hispanicus, RB genome) stems from a hybrid between the marsh frog and the Italian pool frog. Finally, the Graf’s hybrid frog (Pelophylax kl. grafi, RP genome) originated from the hybridization between the edible frog (in which the DNA of the pool frog is eliminated from their gametes) and the Iberian waterfrog.

Schemes by Darekk2 of the hybridogenetic processes in the different European water frog’s kleptons. The bigger circles represent the individual’s genome and the smaller circles the gametes’ genetic material.

As we can see, the genetic information of the marsh frog is the only one present in all three kleptons. These kleptons delete the genetic material of the species with which they share their habitat from their gametes but keep the genetic material of the marsh frog (R). So for example, the edible frog (P. kl esculentus) deletes form its eggs the DNA of the pool frog (L) with which it encounters and breeds in its natural range, resulting in more edible frogs (RL). The marsh frog seldom reproduces with some of its hybrids and if it does, they produce normal marsh frogs.

SALAMANDERS WITH SEVERAL GENOMES

The salamanders of the Ambystoma genus, usually known as mole salamanders, are a genus endemic of North America and are the only living representatives of the Ambystomatidae family. Five of these species form what is known as the “Ambystoma complex”, in which these species contribute to the genetic composition of a unisexual lineage of salamanders which reproduce by gynogenesis (gynoklepton). Based on the mitochondrial DNA of the unisexual populations, it is thought that this complex originated from a hybridization event of about 2.4-3.9 million years ago.

This complex consists of the five following species: the blue-spotted salamander (Ambystoma laterale LL genome, photo by Fyn Kynd Photography), the Jefferson salamander (Ambystoma jeffersonianum JJ genome, photo by Vermont Biology), the small-mouthed salamander (Ambystoma texanum TT genome, photo by Greg Schechter), the streamside salamander (Ambystoma barbouri BB genome, photo by Michael Anderson) and the tiger salamander (Ambystoma tigrinum TiTi genome, photo by Carla Isabel Ribeiro).

In the gynogenesis of this all-female lineage, the egg needs activation by a sperm to start division and development but, it first has to duplicate its genetic material by endomitosis to avoid the formation of an unviable haploid (with half the genetic information) zygote. Yet, as in parthenogenetic reptiles, in the long term the lack of genetic recombination can take its toll on the individuals. That’s why this lineage of unisexual salamanders has the capacity of occasionally incorporating the whole genome from the males of four of the species which constitute the complex (currently the reproduction of streamside salamanders with members of the unisexual lineage hasn’t been documented).

Scheme from Bi, Bogart & Fu (2009) in which we can see the different paths that the gynogenetic mole salamanders can take while reproducing.

These individuals don’t mix the newly acquired genome, they add it. Therefore, among the members of this lineage we can find diploid, triploid, tetraploid and even pentaploid individuals (even if as the ploidy increases the individuals are less apt to survive) depending on how many different genomes the previous generations had incorporated.

Among the klepton, the most common genome combination is that of triploids based on the blue-spotted salamander and the Jefferson salamander, with the genomes LLJ (left, image by David Misfud) and JJL (right, image by Nick Scobel), even though the number of combinations is incredibly large. For this reason why scientists haven’t been able to decide a valid scientific name for this group of hybrid origins.

Unlike the water frogs, it is very difficult to define a scientific name for the klepton inside Ambystoma, as the genomes of the different species can be found in different combinations and proportions in different unisexual individuals.

REFERENCES

The following sources have been consulted during the elaboration of this entry:

• Halliday & Adler (2007). La gran enciclopedia de los Anfibios y Reptiles. Editorial Libsa.
• Masó & Pijoan (2011). Anfibios y Reptiles de la Península Ibérica, Baleares y Canarias. Ediciones Omega.
• Alain Dubois (2011). Species and “strange species” in zoology: Do we need a “unified concept of species”?. Comptes Rendus Palevol. Vol 10. Pp: 77-94.
• Bogart, Bi, Fu, Noble & Niedzwiecki (2007). Unisexual salamanders (genus Ambystoma) present a new reproductive mode for eukaryotes. Genome. Vol 50. Pp: 119-136.
• Bi, Bogart & Fu (2009). An examination of intergenomic exchanges in A. Laterale-dependent unisexual salamanders in the genus Ambystoma. Cytogenetic and Genome Research. Vol 124. Pp: 44-50.
• Cover photo by Dave Huth.

Nutritional genomics: À la carte menu

When Hipprocrates said “let food be your medicine and medicine be your food” he knew that food influences our health. And it tells us that nutritional genomics, which I will discuss in this article; a new science appeared in the post genomic era as a result of the sequencing of human genome (all DNA sequences that characterize an individual) and the technological advances that allow the analysis of large amounts of complex information.   

WHAT IS NUTRITIONAL GENOMICS?

The aim of nutritional genomics is to study the interactions of genes with elements of the human diet, altering cellular metabolism and generating changes in the metabolic profiles that may be associated with susceptibility and risk of developing diseases.

This study wants to improve the health and to prevent diseases based on changes in nutrition. It is very important not understand nutritional genomics how that specific food or nutrients cause a particular answer to certain genes.

When we talk about diet we have to distinguish between what are nutrients and what are food. Nutrients are compounds that form part of our body, while foods are what we eat. Food can take many nutrients or only one (such as salt).

NUTRIGENOMICS vs. NUTRIGENETICS

Within nutritional genomics we find nutrigenomics and nutrigenetics, but although their names we may seem to mean the same is not the case (Figure 1).

Nutrigenomics is the study of how foods affect our genes, and nutrigenetics is the study of how individual genetic differences can affect the way we respond to nutrients in the foods we eat.

Figure 1. Schematic representation of the difference between nutrigenomics and nutrigenetics (Source: Mireia Ramos, All You Need is Biology)

NUTRIGENOMICS IN DETAIL

Nutrients can affect metabolic pathways and homeostasis (balance) of our body. If this balance is disturbed chronic diseases or cancer may appear, but it can also happen that a disease, which we have it, be more or less severe. It means that impaired balance can give the appearance, progression or severity of diseases.

The aim of nutrigenomics is that homeostasis is not broken and to discover the optimal diet within a range of nutritional alternatives.

Thus, it avoids alterations in genome, in epigenome and/or in expression of genes.

ALTERATIONS IN GENOME

Free radicals are subproducts that oxidise lipids, proteins or DNA. These can be generated in mitochondria, organelles that we have inside cells and produce energy; but we can also incorporate from external agents (tobacco, alcohol, food, chemicals, radiation).

In adequate amounts they provide us benefits, but too much free radicals are toxic (they can cause death of our cells).

Antioxidants neutralize free radicals. But where can we get these antioxidants? There are foods that contain them, as Table 1 shows.

Table 1. Example of antioxidants and some foods where we can find them (Source: ZonaDiet)

The way we cook food or cooking is important for avoid to generate free radicals. In barbecues, when we put the meat on high heat, fats and meat juices fall causing fire flames. This produces more flame and it generates PAHs (a type of free radicals). These adhere to the surface of the meat and when we eat it can damage our DNA.

ALTERATIONS IN EPIGENOME

Epigenome is the global epigenetic information of an organism, ie, changes in gene expression that are inheritable, but they are not due to a change in DNA sequence.

Epigenetic changes may depend on diet, aging or drugs. These changes would not have to exist lead to diseases as cancer, autoimmune diseases, diabetes…

For example, with hypomethylation, in general, cytosines would have to be methylated are not. What does it mean? Hypomethylation silenced genes and then, they cannot be expressed. Therefore, we need methylated DNA. A way of methylate DNA is eating food rich in folic acid.

ALTERATIONS IN GENE EXPRESSION

There are agents (UV rays) that activate pathways that affect gene expression. Occurring a cascade that activates genes related to cell proliferation, no differentiation of cells and that cells survive when they should die. All this will lead us cancer.

It has been found that there are foods which, by its components, can counteract activation of these pathways, preventing signal transduction is given. For example curcumin (curry), EGCG (green tea) or resveratrol (red wine).

 REFERENCES

• The NCMHD Center of Excellence for Nutritional Genomics
• Michael Müller’s Laboratory
• Documentos TV: La Alimentación del Futuro
• M. Müller, S. Kersten. Nutrigenomics: Goals ans Strategies. Nature Reviews Genetics 2003; 4, 315-322
• J. Kaput, R.L. Rodríguez. Nutritional Genomics: the Next Frontier in the Postgenomic Era. Physiol Genomics 2004; 16, 166-177
• J.M. Ordovas, D. Corella. Nutritional Genomics. Annu Rev Genomics Hum Genet 2004; 5, 71-118
• Portal Antioxidantes
• Main picture: The Pu·rée

Why I look similar to my parents?

The reason of the similitude with our parents is genetics. This science studies the inheritance; it means how offspring resemble their parents, the diseases that are transmitted from generation to generation… It is biology’s discipline growing quickly and it affects biology, healthy and society in general. In this article I am going to talk about what is genetics and the DNA’s discovery.

HOW GENETIC INFORMATION IS INHERITED?

The genetic information is inherited to the offspring by genes, which are the storage unit of this information. They are located inside the chromosomes and they occupy specific positions. The number of chromosomes is constant inside species, but different between other species.

In humans the number of chromosomes is 46. In each cell we have 46 chromosomes, which 44 are autosomal, i.e., not a chromosome sexual and 2 chromosomes sexual. The total of 46 chromosomes is the human genome.

Our genome consist of 2 sets of 23 chromosomes counterparts. This means that each set have the same characteristics respect the other set and one comes from our mother by ovum and the other one comes from our father by sperm (Figure 1). Inherit each set of our progenitor is the reason why we resemble they, but also is via that we inherit some genetic diseases.

Figure 1. Human female karyotype, i.e., the graphical representation of chromosomes. They are placed in pairs sorted and size, from the largest to the pair smaller, plus the sex chromosomes (Source: Mireia Ramos, Cerba Internacional SAE)

CHEMISTRY OF GENES

Genes are parts of DNA (deoxyribonucleic acid), comprising by the join of small molecules that called nucleotide. These nucleotides contain a pentose (compound of 5 carbon), a phosphate and a nucleobase (organic compound with an atom of nitrogen) (Figure 2). There are 4 nucleobase: two purines (adenine and guanine) and two pyrimidines (thymine and cytosine). These nucleobases distinguish each nucleotide and their arrangement constitutes the genetic code.

Figure 2. Details of the chemistry of DNA (Source: Eduredes: Los ácidos nucleicos)

But all knowledge about DNA and genes is recent. The structure of DNA was discovered by James Watson and Francis Crick in 1953 in Cambridge (Figure 3). Previously, other scientists had done studies to try to determine the similarity between relatives, but it was not until this discovery it was understood that there was chemistry behind it.

Figure 3. Francis Crick (right) and James Watson (left) with the construction of the structure of DNA (Source: The DNA store)

THE BEGINNING OF THEIR STORY

Watson, an American 23 year-old biologist, and Crick, an English 35 year-old physicist, worked in the Cavendish Laboratory in Cambridge. They spent many months building models of molecules and comparing them to the information they had, but still they couldn’t find the correct structure of DNA.

In the King’s College of London, the physicist Maurice Wilkins and Rosalind Franklin, another physicist with knowledge in crystallography. She took X-ray pictures of DNA (Figure 4).

Figure 4. The four people who contributed to the discovery of DNA (Source: Biology: The people responsible for the discovery of DNA)

Watson and Crick, after present a wrong model of the triple helix, told Maurice Wilkins about what they were trying to do and he showed them a new and better X-ray picture of DNA, which had been taken by Rosalind Franklin, without her permission. This was the picture number 51 to help them solve the mystery (Figure 5).

Figure 5. Explanation of picture 51 that used Watson and Crick (Source: Seguramente estaré equivocado: La “fotografía 51”)

When the university’s Cavendish Laboratory was still at its old site at nearby Free School Lane, the pub was a popular lunch destination for staff working there. Thus, it became the place where Francis Crick interrupted patrons’ lunchtime on 28th February 1953 to announce that he and James Watson had “discovered the secret of life” after they had come up with their proposal for the structure of DNA. This day is called for someone the 8^th day of Creation.

The 25^th April 1953 it published their article with 900 words in Nature (Figure 6). Three years earlier had published law Chargaff, which was one of the foundations to apply the theory of the double helix of DNA. This law establishes the complementarity of the bases in DNA, i.e., adenine (A) pairs with thymine (T) and the same with guanine (G) and cytosine (C) (Figure 2). So the amount of purine (A and G) is equal to the amount of the pyrimidine (T and C).

Figure 6. Article published in the journal Nature, which shows the picture 51 (Source: The DNA store)

THE IMPORTANCE OF GENETICS

It has been argued that the discovery of DNA as well as our understanding of its structure and function may well be the most important discovery of the last century. The effect of the discovery of DNA on scientific and medical progress has been enormous, whether it involves the identification of the genes that trigger major diseases or the creation and manufacture of drugs to treat these devastating diseases. In fact, the identification of these genes and their subsequent analysis in terms of therapeutic treatment has ultimately influenced science and will continue to do so in the future.

While the discovery of DNA has been a significant one in the twentieth century, it will continue to revolutionize medicine, agriculture, forensics, paternity and many other important fields in society today. DNA research encompasses an evolving area of progress and continued funding and interest in its relevance will likely fuel new discoveries in the future.

REFERENCES

• Course notes of Genetics, Bachelor’s Degree (UAB)
• Universitat Autònoma de Barcelona: Genetic’s Degree
• Proyecto Biosfera: La materia viva
• The Guardian: DNA double helix
• Explore DNA

Communication among plants: allelopathy

As always have been said, plants are unable to speak. But, even if they don’t speak, this does not mean they do not communicate with each other. Relatively few years ago, during the period from 1930 to 1940, it was discovered that plants also transmit certain stimuli to others. But, what kind of communication exist among them? What are their words and how are pronounced? And what involves this interaction?

INTRODUCTION

In 1937, Molisch introduced the term allelopathy referring to the two Latin words “Allelon” and “Pathos”, which mean “another” and “suffering”, respectively. But, the actual meaning of the word was determined by Rice in 1984. Allelopathy now means any effect that a plant transmits to another directly or indirectly through production of different metabolism compounds, causing either a positive or negative effect on the other organism. These compounds are called allelochemicals.

The allelochemicals are released on the environment by plants. But, they are not directly aimed to the action site, thus it is a passive mechanism. To be effective, allelopathic interaction needs that these substances are distributed along the ground or the air and that they reach the other plant. Once inside the recipient plant, this one may have defense and degradation mechanisms of the compounds while avoiding the effect, or conversely, it will suffer a pathological effect.

Allelopathy (Adapted image of OpenClips)

ROUTES OF RELEASE

The release of allelochemicals can be 4 main ways:

• Leaching: the aerial part of the plant lets go substances by rain effect. Then, they can fall on other plants or on the ground. Therefore, it can be direct or indirect effect, depending on whether they falls on another plant or not. Although, in principle, it is considered indirect.
• Decomposition: the plants drop their leftovers on the ground, where they decomposed under the microorganisms action, which help the release of the compounds. The plant leftovers range from leaves to branches or roots. The substances found there may be inactive until coming into contact with moisture or microorganisms, or can be active and then be inactivated by the microorganisms activity or by being retained on the ground. So, it is an indirect way. The decomposition is very important because the most of allelochemicals are released this way.
• Volatilization: the substances are released by the stomata (structures that allow the exchange of gas and transpiration). These are volatile and water-soluble, thus can be absorbed by other plant’s stomata or be dissolved in water. Commonly, plants using these pathways occur in temperate and warm climates. It is considered a direct route.
• Exudation: the plants can also release allelochemicals directly by live roots. The exudation system depends especially of roots state, of the kind of roots and of their growing level (if they are growing or not).

The 4 main pathways of allelochemical releasing: volatilization (V), leaching (L), descomposition (D) and root exudation (E). (Adapted image of OpenClips)

REGULATORY FACTORS

Factors influencing the release of allelochemicals are normally abiotic, such as high radiation, low humidity, unsuitable pH, ultraviolet light, temperature, nutrient deficiency, pollution or contamination (including pesticides ). The higher is the stress caused by this factors to the plant, highest is the allelochemicals amount released from secondary metabolic routes.

• This is important for research and pharmacy: for generating relevant oils many plants are grown under stressful conditions, as it is thanks to the production of these secondary metabolites that they can survive.

Furthermore, biotic factors also take part, such as insects, herbivores or competition with other plant species. These activate the plant defenses and then the organism is stimulated to secrete bitter substances, or substances that harden the tissues, that are toxic or give off unpleasant odors, etc.

Finally, each plant has its own genome and this makes synthesize those or other substances. But, they are also determined by the phenology (life stages) and the development (if the size of the plant is bigger, it can release more allelochemicals).

ACTION MODE

The allelochemicals are very diverse and, therefore, it’s difficult to establish a general action model; since it depends on the compound type, the receiving plants and how it acts.

When we talk about how the allelochemicals can act at internal level, there is a large number of physiological parameters that can be affected. They have action on the cellular membrane, disrupt the activity of different enzymes or structural proteins or alter hormonal balance. They can also inhibit or reduce cellular respiration and chlorophyll synthesis, leading to a reduction in vitality, growth and overall development of the plant. Furthermore, these substances can also reduce seed germination or seedling development, or affect cell division, pollen germination, etc.

On the other hand, at external level, the allelochemicals may be related to the release or limitation of nutrients that are found in the soil. Others act on microorganisms, leading to a perturbation on the symbiotic relationships they establish. In addition, these substances have great importance into the generations succession, as they determine certain competition tendencies and also act on the habitat ecology. Even so, it is a successive competition, as they do not directly compete to obtain the main resources.

EXAMPLES

One of the best known allelochemicals is the juglone, produced by the Eastern black walnut (Juglans nigra). Juglone, once released to soil, can inhibit the other plants growth around the tree. This allows the issuing organism to get more resources, avoiding competition.

Eastern black walnut  (Juglans nigra) (Photo taken by Hans Braxmeier)

A very curious case is that of the acacias (Acacia). These plants synthesize a toxic alkaloid that migrates to the leaves when the body is attacked by a herbivore. This substance’s toxicity is high, because it damages with the contact and ingestion, becoming deadly even for large herbivores.In addition, this alkaloid is volatile and transferred by air to other nearby acacias, acting as an alarm. When the other acacias receive this signal, this component is segregated to leaves, making them darker. Even so, the effect is temporary. This makes animals like giraffes have to constantly move to eat a few leaves of each acacia, and always against the wind, to avoid toxicity.

Acacias (Acacia) (Photo taken by Sarangib)

REFERENCES

• A. Aguilella & F. Puche. 2004. Diccionari de botànica. Col·leció Educació. Material. Universitat de València: pp. 500.

• A. Macías, D. Marín, A. Oliveros-Bastidas, R.M. Varela, A.M. Simonet, C. Carrera & J.M.G. Molinillo. 2003. Alelopathy as a new strategy for sustainable ecosystems development. Biological Sciences in Space 17 (1).
• J. Ferguson, B. Rathinasabapathi & C. A. Chase. 2013. Allelopathy: How plants suppresss other plants. University of Florida, IFAS Extension HS944
• Notes of Phanerogamae, Applied Plant Physiology and Analisi of vegetation, Degree of Environmental Biology, UAB