Feeling our way through the transposons Maize

Maize was where it all began in the 1940’s when Barbara McClintock discovered transposable elements (TE’s) in the popular cereal grain, and Maize is again at the forefront of transposons studies.

The Maize kernel has been ideal for studying the interaction between TE’s and host genomes because kernels on a maize ear show unstable phenotypes due to interplay between a TE and a gene that encodes an enzyme in the pigment biosynthetic pathway.

While debate continues whether TE’s are agents of evolution or parasitic passengers, SanMiguel et al. has provided evidence, for the first time, that TE’s can rapidly restructure a genome. Over the past 3 million years the Maize genome has doubled in size due to a burst in retrotransposon activity. The study determined the insertion dates for 17 of the 23 retrotransposon found near the maize adh1 gene and discovered that retrotransposon insertions have increased the genome size from approximately 1200 Mb to 2400 Mb!

Was this flurry of activity a response to stress? This would be consistent with the genome restructuring role envisioned by McClintock all those years ago. Continuing down this line of research has the potential to provide mechanisms that will explain how evolution works and a molecular level.

Submitted by: s4123804

Control of Flowering and Cold Adaptation in Plants

The Flowering Locus C (FLC) , which represses flowering, in Arabidopsis thaliana is negatively regulated by the FVE and FLD genes, which work in a histone deacetlyase complex. High levels of FLC expression were found in fld and fve mutants. This indicates that FVE and FLD work to repress FLC by means of deacetylation.

In cold temperatures, plants, express several genes to prevent injury. A DNA element responsible for inducing an array of cold-induced genes is C/DRE. A mutant in a plant with delayed flowering, acg1, had multiple copies of C/DRE. This mutation was discovered to be in the FVE allele. It was deduced that FVE would also repress the production of cold-induced genes by deacetylation.

It was further found that wild-type plants had flowering delayed when subjected to cold but this was not the case in fve mutants. Based on that, a conclusion was made that FVE regulates both flowering time and cold acclimatisation and is useful in adapting to changing spring weather.
Although fve mutants affect the expression of cold-induced genes, fld mutants do not. The author surmised that FVE worked in complex with FLD to repress FLC but worked independently to repress the expression of cold-induced genes.

References:

Amasino, R. 2004. Take a Cold Flower.
Nat. Genet. 36 (2) 111 -112.

Kim, H-J et. al. 2004. A genetic link between cold responses and flowering time through FVE in Arabidopsis thaliana.
Nat. Genet. 36 (2) 167-171.

Submitted by: 41352328

Are antibiotics doing more harm than good?

Directed Evolution - SOS
Submitted by: 41287925


The efficiency of antibiotics to cure infections has waned over the years as bacteria strains evolve antibiotic resistance. Studies on Staphylococcus aureus have shown that mutations in the gene were self-induced. When the bacterium was under environmental stress (e.g. UV damage and antibiotics), it upregulated genes to repair DNA damage.. This response was coined the SOS response. The SOS response, mainly initiated by derepressing LexA protein via the RecA protein, gives rise to mutations which allows evolution of immunity towards antibiotics. The persistence of bacteria in the host often proves to be fatal.

Another caution of antibiotic usage involves pathogenicity islands on Staphylococcus aureus. Treatment of the bacterium with SOS-response inducing antibiotic, β-lactam, resulted in staphylococcal prophage induction in S. aureus lysogens and replication and high-frequency transfer of pathogeneticity islands. Such antibiotic inadvertently promotes the spread of virulence factors, doing more harm than good in the body.

As bacteria are evolving greater resistance in response to antibiotic therapy, humans have to race ahead in search of newer, more effective drugs, while exercising caution in using SOS response-inducing antibiotics. I wonder, how long more can we stay ahead before the evolution of drug resistance eventually catches up?


References:
1) Elisa M, Carles Ú, Susana C, Noelia S, Íñigo L, Richard P. N, Jordi B, José R. P. (2006)
ß-Lactam Antibiotics Induce the SOS Response and Horizontal Transfer of Virulence Factors in Staphylococcus aureusJ. Bacteriol. 188(7): 2726-2729
http://jb.asm.org/cgi/content/full/188/7/2726?maxtoshow=&HITS=10&hits=10&RESULTFORMAT=&searchid=1&FIRSTINDEX=0&volume=188&firstpage=2726&resourcetype=HWCIT


2) Ryan T. C, Marcus B. J,Neill A. G, Timothy D. M, Behnam J,
Scott N. P, Floyd E. R (2007) Complete and SOS-Mediated Response of Staphylococcus aureus to the Antibiotic Ciprofloxacin. Bacteriol. 189(2): 531–539
http://jb.asm.org/cgi/content/full/189/2/531?maxtoshow=&HITS=10&hits=10&RESULTFORMAT=&searchid=1&FIRSTINDEX=0&volume=189&firstpage=531&resourcetype=HWCIT


3) Cirz R.T, Chin JK, Andes DR, de Crécy-Lagard V, Craig WA, et al. (2005) Inhibition of Mutation and Combating the Evolution of Antibiotic Resistance. PLoS Biol. 3(6): e176
http://biology.plosjournals.org/perlserv/?request=get-document&doi=10.1371/journal.pbio.0030176

Heat-shock proteins - Hidden Evolution

How far does the human understanding of evolution reach?

Speculation based on some recent research suggests we may have only scratched the surface. The theory concerns the period of rapid divergent evolution known as the Cambrian explosion, which was a period of 100 million years in which the vast majority of body forms evolved, and none have evolved since. One theory suggests this oddity may have been caused by uncovering hidden variation, recently revealed to be kept in check Heat-Shock Proteins (HSP’s). Until recently, it was understood that these proteins were used to buffer against external stresses, such as heat of pH change, in all cells. Now, however, research shows that they work to buffer against powerful internal stress: genetic variation.

The research shows that by warping or removing these Heat-Shock Proteins, genetic variation was increased in both D. melanogaster (a fly) and A. thaliana (a plant) over the course of a single generation. The distinction between plant and animal shows that this phenomenon is not unique to one or the other, but likely present in all organisms (as all organisms make use of Heat-Shock Proteins). It is not yet certain that this an accurate beginning for a model of evolutionary leaps, but it is certainly a start.

References:

http://www.nature.com.ezproxy.library.uq.edu.au/news/1998/981203/full/981203-3.html

http://www.nature.com.ezproxy.library.uq.edu.au/news/2002/020506/full/020506-13.html

Transposable Elements and Evolution of Mammals

Directed evolution: Transposable elements.
submitted by: 41161351

Transposons (TEs) or 'jumping genes', and sequences derived from transposons, make up a considerable proportion of the genomes of all organisms. There is evidence which suggests that TEs are derived from retroviruses which have become incorporated into the genomes of their hosts. While most TE derived DNA is of unknown function, some protien coding genes have been shown to be derived from TEs and retroviruses. Recent studies done which look at the evolution of mammals, in particular primates and homonids, suggest that TEs may have played an important role in the evolution of humans. It appears that there still are transposons active in the human genome which may contribute to both disease and genetic variatation. Transposon-derived DNA sequences are proving useful in assessing the genetic relationships between organisms, even within populations of a species. If you're interested in finding out more go to:

http://www.springerlink.com/content/erhbgtt39fuxyr9t/fulltext.pdf

or

http://www3.interscience.wiley.com/cgi-bin/fulltext/69502244/PDFSTART

or

http://www.biomedcentral.com/content/pdf/1471-2148-4-38.pdf

Winter doesn’t kill plants, It makes them grow!

So how do plants know to flower in the spring time when conditions are optimal and there is a higher chance for survival?

The answer lies within the winter before. In some species, such as model organism Arabidopsis sp. the promotion of flowering in the spring can only occur after prolonged exposure to the cold temperatures of winter. This response to stimuli is known as vernalisation and it affects many other species in many different ways. Some may commence flowering right after the winter ends, and others can take more then half a year post vernalisation. The effect of the cold treatment can also depend on the stage of the plants life cycle, some will show no response until they reach a certain height, and others can be verbalized as seeds.

The molecular process behind vernalisation is still not completely understood and is still the focus of many current studies. Progress so far has uncovered that the ecological stimulus of cold temperatures are directly related to the increased production of the FLC gene (flowering locus C), which has identified it as a floral inhibitor. As winter comes to pass and warmer temperatures return, the expression of FLC is downregulated, and the plant is allowed to proceed to flower.

Primary Reference:
Michaels S. D., Amasino R. M. (2000) Memories of winter: Vernalization and the competence to flower. Plant, Cell and Environment 23 (11), 1145–1153.

Supporting article:
Dimech A. (2004) Vernalisation: Cold Temperature Exposure

Student ID: 41178171

A Genentic Explanation for Stroke.

Chromosomal mapping of quantitative trait loci (QTL) contributing to stroke in a rat model of complex human disease.

What causes the stroke? Is it entirely due to mechanical end organ damage, or is there any hidden genetic basis as it is increasingly the case for most other diseases? Sperenza and collages from Brigham and Women's Hospital in Boston carried out an experiment to understand genetic basis of stroke and identify genes related.

Two inbred mice strains; stroke-prone spontaneously hypertensive rat (SHRsp) and stroke-resistant spontaneously hypertensive rat (SHRsr); were crossed and the hybrid progeny were subjected to a total genome scan.

Three QTLs were identified on different chromosomes, which contributed to 28% of genetic variation associated with stroke. They were named as STR1, STR 2 and STR3; where the first locus accounts for 17% of overall variance. Human and mouse genetic maps of the relevant QTL regions were compared to that of rat, in order to identify any possible candidate genes for above mentioned loci. STR1 and STR 3 showed no colocalisation, but STR 2 showed similarities to human atrial natriuretic factor gene, which is located immediately adjacent to the brain natriuretic factor gene. Both these genes could be candidate genes of the QTL loci, showing major influence on vascular conditions, hence contributing to stroke.

This study is not only significant in demonstrating the strength of using correct animal models to study complex traits, but also in challenging the common concept that stroke is basically attributed to mechanical end-organ damage due to long-term hypertension.

References.

Rubattu S, Volpe M, Kreutz R, Ganten U, Ganten D, and Lindpaintner K. (1996) Chromosomal mapping of quantitative trait loci contributing to stroke in a rat model of human disease. Nat Genet 13: 429–434.

SOS control of mutation and virulence in EPEC

The SOS response is a last ditch effort for survival by a pathogen when subjected to DNA damage.  It involves the activation of numerous genes that are normally repressed causing accelerated mutation.  This is all achieved through the use of DNA polymerases that are naturally more error prone and so mutate the genetic code far more quickly.  You can find out all about the mechanism of the SOS response here.

A recent study has shown that LexA, the master switch for the SOS response, is involved in controlling effector proteins crucial for Enteropathogenic Escherichia coli (EPEC), the main cause of watery diarrhea, to attach to the intestinal wall and then secrete proteins into the host cell.  Why is this important?  Because it can be seen that there is a coordinated response by this pathogen to increase its chances of survival both by mutating to protect itself from any barrage the body or antibiotics can through at it, as well trying to increase its chances of infection by producing more toxic compounds.  Now that is one smart (and scary) bacterium! 

Posted by:  Connor Skennerton (41192373)

 References:

1. Jay L Mellies, Kenneth R Haack, and Derek C Galligan (2007). €œSOS regulation of the type III secretion system of enteropathogenic Escherichia coli, Journal of bacteriology 189, no. 7: 2863-72.
2. Ryan T Cirz et al. (2005) €œInhibition of Mutation and Combating the Evolution of Antibiotic Resistance,€ PLoS Biology 3, no. 6: e176, http://dx.doi.org/10.1371%2Fjournal.pbio.0030176.

TEEM Theory: A paradigm shift of revolutionary proportions?

What is it that makes instinct? How is it that most animals have the ability to identify predators and prey without prior knowledge? How does a bird 'just know' how to build a nest or seduce a female with a complex mating ritual? These complex, innate behaviours are unexplainable by Mendelian inheritance. To date there is no agreement as to how these and many other innate behaviours were first encoded into an organism's genes, nor how they are inherited.

The Trauma-Encoded Emotional Memory (TEEM) theory postulates that within the DNA code of eukaryotes, there are not one but two distinct modes of inheritance. One being the mendelian-inherited expression of genes through their transcription to RNA and translation to protein in accordance with the central dogma; it is this system which we understand to be reponsible for the evolution of phenotypic traits. The other involves elements of noncoding DNA (ncDNA), formerly known as 'junk' DNA, which are inherited in a non-Mendelian fashion and may be responsible for the evolution of behavioural traits.

In metazoans, ncDNA is present as a relatively large proportion of the DNA code and numerous studies have now shown that these noncoding regions are highly conserved in a wide range of species. This has further led to the proposal that the amount of ncDNA present in an organism's DNA is a more valid measure of the organism's behavioural complexity than the number of protein-coding genes. TEEM Theory, or Teemosis, suggests that these noncoding regions of DNA are environmentally acquired units of adaptive information expressed as emotion and are the basis for emotional responses, innate behaviour and instinct.

Wheras protein-coding genes are largely resistant to environmental effects, the Teemosis Inheritance System (TIS) is triggered by non-lethal environemtal stressors. Any event brought about by an environmental stressor, usually a negatively associated event such as a predator attack or misadventure, but also positive events such as a mating event, which produces an emotional response of sufficient intensity to temporarily destabilise the homeostasis of the central nervous system and stimulate the hypothalamic-pituitary-adrenal axis will increase the mutational activity of transposable elements, or transposons. This mutational activity may involve the duplication, deletion, rearrangement, and transposition of nucleotide sequences in ncDNA into new sequences which correspond to the stressor emotions. The new sequences of nucleotides do not behave as triplet codons as in those of the Universal Genetic Code, but rather behave more linguistically as rearrangeable units of 1 to 6 nucleotides in length. Each event which triggers the TIS produces its own unique linguistic sequence.

The Teemosis hypothesis argues that all instincts and innate behaviours in animals are ancestrally genetically encoded and heritable elements of ncDNA which are expressed as emotional responses to certain situations. If confirmed, the TEEM theory has the potential to create a paradigm shift in our understanding of the functioning of ncDNA, behaviour and genetic diseases which is nothing short of revolutionary.