Multiple choice: how histone mods help choose where to splice

Humans can make about 100,000 different proteins with a mere 20,000 genes. How is this possible? The trick is in a process called alternative splicing, where the inclusion of different exons in mature mRNA allows the production of multiple proteins from a single gene.
The splicing machinery needs to recognise which exons to keep amongst the vast expanses of intronic sequences. So how does the splicing machinery choose where to do its job? A recent study by Luco and colleagues has proposed an answer and it involves histone modifications.
The researchers used an established model of alternative splicing, the human FGFR2 gene. The splicing that occurs in 2 different cell types leads to either exon IIIb or exon IIIc being included in the mRNA. They mapped the histone mods over the FGFR2 gene in both cell types and found that the amount of H3K36me3 was vastly increased in the cell type where exon IIIb is repressed. So the researchers tried to figure out how H3K36me3 affects the splicing outcome.
Their experiments led to the identification of a three part system made up of H3K36me3, a protein that binds to it, and the splicing regulator that represses exon IIIb.
Find out the fascinating details at http://www.sciencemag.org/cgi/content/abstract/327/5968/996

Astrid Vekemans 4239 6990

link between NNK and induces DNMT1

This study provides an explanation between the compounds found in cigarette or what is known as NNK ( nicotine ,nitrosamine and ketone) and the lung cancer, and what is the main causes to make NNK increase DNMT1 protein expression and activity? It also shed the light on over expression of DNMT1 protein stability through AKT signalling. It besides trigger off AKT then inhibits GSK3β/β-transducin repeat (include protein) mediated protein degradation, and the result DNMT1 protein accumulation.
It can be reason out that the conclusions made in this study are highly pertinent to the study of other Kind of cancer. It can be reason out that the conclusions made in this study are highly pertinent to the study of other Kind of cancer. The results showed assertions of this research provide an invaluable perspective in tumour and cancer research as well as studies on other types of human disease. It also opens up probability for developing better Means in improving prognosis in clinical manifestation of related epigenetic disorders that lead to these diseases.

Ahmad Baqazi

41606629

Review of induction of flowering by DNA demethylation in Perilla frutesencs and Silene armeria

YueLin LIU

42179054

The flowering process of many plants is regulated by gene expression, gene modification and/or environmental factors, such as temperature, night length and stress (K.C. Wada, et al, 2010). When talking about the gene modification, DNA methylation is always a crucial factor which is related to the plants’ vernalization. And also the methylation of DNA is a part of the epigenetic control. So in this research experiment, the authors focused on the cytidine analogue 5-azacytidine (azaC), which is commonly known as a methyltransferase inhibitor (C. Stresemann, et al, 2006), induced two kinds of plants, Perilla frutescens and Silene armeria, in order to find out the relationship between vernalization and DNA methylation and the heritability of the azaC induced effect in the offspring. What is more, they used methylation sensitive amplified fragment length polymorphism (MS-AFLP) analysis in these two plants so that the alterations of the DNA methylation states could be detected by changing the photoperiodic conditions.

Reference: Hiroshi Kondo, Takeshi Shiraya, Kaede C. Wada, Kiyotoshi Takeno. (2010). Induction of flowering by DNA demethylation in Perilla frutescens and Silene armeria: Heritability of 5-azacytidine-induced effects and alteration of the DNA methylation state by photoperiodic conditions. Plant Science, 178, 321-326

Is Epigenetic Status of Cancer Cells Influence Telomere Length?

Is Epigenetic Status of Cancer Cells Influence Telomere Length?


Telomeres are specialised chromatin structures essential for chromosome end protection and chromosomal stability are located at the end of the eukaryotic chromosomes and contain DNA sequences that are repeated many times. In normal (non-cancerous) human somatic cells telomere contain about 500 to 3000 TTAGGG repeats and are gradually shorten with age whereas in cancer cells do not shorten with age. It has also been found that cells with longer telomere length survive longer and go through more cell divisions than cells with shorter telomeres.

In recent studies it is found that in more than 90% of all cancer types in human tumours there is an increase in telomerase activity, an enzyme involved in regulation of telomere length. This shows that a certain minimum length of telomeres is necessary to maintain in order to sustain tumour growth. Thus one of the ways to combat cancer is to control telomere length by inhibiting telomerase activity and also other possible mechanisms that regulate telomere length in cancer cells.

REFERENCE:

Vera, E, Canela, A, Fraga, MF, Esteller, M & Blasco MA 2008, ‘Epigenetic regulation of telomeres in human cancer’, Oncogene, vol. 27, no. 54, pp. 6817-6833.

Jameris Dkhar
42256049

Disturbs of brain development can lead to adult to adult behavioral deficits, let’s check it out!

The neuronal network formation during development influences adult brain function, so that any disturbance at this stage is suggested to trigger the pathology of adult mental disorders. On the basis of this fact, the consequences of knocking down genetic susceptibility factors, for disorders such as schizophrenia, have been elucidated by the present study.

By using an innovating technique – In Utero Gene Transfer – this research group modulated the expression of target genes in the prefrontal cortex, and then they follow the development of the brain and how these changes may influence high brain functions as cognition and information processing.

In order to follow these changes from early brain development to postnatal brain maturation mice with selective knockdown were generated in this study. The importance of the use of animal models is also shown in this research, as these models can help us to be clear in aspects such as the consequences in high brain functions in adults of the disturbances in early development.

REFERENCE: M. Niwa, et al. Knockdown of DISC1 by In Utero Gene Transfer Disturbs Postnatal Dopaminergic Maturation in the Frontal Cortex and Leads to Adult Behavioral Deficits. Neuron, Volume 65, Issue 4, Pages 480-489

Maria Cristina Rondon

42142012

Changes in DNA methylation after exposure to traffic pollution.

Air pollution has been known for a long time to have a significant detrimental effect on the health of many organisms, including humans. Airborne particulates have been linked to cardiovascular diseases, with increases in mortality in relatively short time periods after unusually high incidences of pollution. In separate research, decreases in methylation in blood DNA have been linked to forms of cardiovascular stress. It follows that there may be some observable link between these two separate observations. In this study, a group of scientists from around the world have explored the effects of short term air pollution on blood DNA methylation. There investigations include:

• Testing the effect of exposure to different particulates over periods of between 4 hours and 7 days.

• Testing the effect of seasonal and day-of-the-week variation.

• Comparing results over two different forms of DNA methylation.

http://www.ncbi.nlm.nih.gov/pubmed/19136372

Robert Cope
40977649

Food for thought: novel revelations in human DNA demethylation coupled mechanism discovered in fish

             A rapidly evolving focus in research is the understanding of epigenetic (the superficial inheritable mechanisms of DNA modification) factors contributing to development and malignancy. DNA methlylation is one of the key mechanisms by which epigenetics proceeds, through the prevention of specific gene expression. Explicitly, typical DNA methlylation occurs on the 5 position of cytosine nucleotides (5-meC) occupying (60-90% of) CpG spans of genomic sequence (in mammalian somatic cells). Resultant in altering cellular differentiation, phenotypic expression, and other fundamental cellular function, DNA methlylation is documented to be greatly affiliated with perturbations, such as neoplasia and congenital disorders (e.g. Retts syndrome). Although, much is understood regarding the contributing protein factors performing DNA methylation, little is known with regarding the converse demethlyation process. The zebrafish (Danio rerio) is robust vertebrate model for analysis of genetic cellular development in vivo, due to its small size, high fecundity, and simple husbandry. Amenable to transgenic strategies, the ex utero development of transparent embryos allow for ease of phenotypic analysis and genetic manipulation.

             In a revolutionary study conducted by Rai et al., zebrafish embryos, at the one cell stage were microinjected with a 736 bp hyper-methlyated strand of DNA, to monitor methlylation levels. Elucidation through knockdown and overexpression assays provided evidence of a coupled deamination/ glycosylation mechanism for DNA demethylation. Deamination by either activation induced deaminase (AID) or apolipoprotein B RNA-editing catalytic components (Apobec) alters 5-meC into thymine, resulting in a G:T mismatch. Excision of the thymine is promoted by glycosylation via Mbd4 in a proposed base excision repair-like manner. In fact, overexpression studies actually resulted in demethylation of the zebrafish intrinsic genome, as well as the injected methlyated DNA. Furthermore, the non-enzymatic protein, Gaad45, was found to enhance the interactions and efficacy of the two enzymatic groups, thereby promoting demethylation. As a stepping stone, clarifying a previously unknown, fundamental, natural genetic process regulating epigenetics, the findings of this study provide abundant opportunities for future novel therapeutic strategies to currently incurable DNA methlyation-related diseases.

Lauren Klein (Rygier)

42274593

REFERENCES:

Berman JN, Kanki JP, Look AT. (2005) Zebrafish as a model for myelopoiesis during embryogenesis. Exp Hematol. 33: 997-1006.

Delgado S, Gomez M, Bird A, Antequera F. (2001) Initiation of DNA replication at CpG islands in mammalian chromosomes. EMBO J. 17(8): 2426-2435.

Rai K, Huggins IJ, James SR, Karof AR, Jones DA, Cairns BR. (2008) DNA demethylation in zebrafish involves the coupling of a demainase, a glycosylase, and Gadd45. Cell. 135(7): 1201-1212.

Can a father influence his daughter’s maternal behaviour?

Parental imprinting is an epigenetic mechanism that allows the control of gene expression. At the time of conception, the offspring inherits a copy of each autosomal gene from each parent. However, in a small number of genes found in mammals, one of the two inherited alleles is inactivated.

Peg3 is strongly expressed in the hypothalamus, which suggests that parental imprinting would affect behaviour. Champagne, Curley et al. have recently conducted a study on mice models to explore the role of the paternally expressed gen Peg3 in the behaviour of adult female mice. It was found that the expression of the paternally expressed gene Peg3 is critical for regulating mother-infant interactions. Disruption to Peg3 on mice was demonstrated to have deleterious consequences on important features of maternal behaviour such as nursing and licking/grooming of pups during postpartum period.

In humans, it hasn’t been demonstrated yet that Peg3 has the same behavioural effects, however, similarities on the expression and sequence of this gene in both humans and mice suggests that there could not be radical differences on its function.

REFERENCE: Champagne FA, Curley JP, Swaney WT, Hasen NS, Keverne EB. 2009. Paternal Influence on Female Behavior: The Role of Peg3 in Exploration, Olfaction, and Neuroendocrine Regulation of Maternal Behavior of Female Mice. Behavioral Neuroscience 123: 469-480.

Paola Franco

Do you have the X-Factor? Seems like marsupial and monotreme mammals don’t!

               Inactivation of X chromosome in females is nature’s way of playing fair.  Since females have two X chromosomes and male only one, one of the X chromosomes is inactivated in females to prevent over expression of the same chromosome. This is known as dosage compensation and is a common feature in mammals and is one of the best examples of an epigenetic system. The gene responsible for this is the XIST (X-inactive specific transcript) which is present in the X-chromosome inactivation centre. This gene sequence conserved in most of the mammals is missing in non- eutherian (Non-placental) mammals like marsupials and monotreme (egg-laying). Infact on mapping this region scientists not only failed to find this gene but also the region homologus to it.
        This now leaves us with many questions. Since X inactivation is also seen in non-eutherian mammals if not XIST then what controls it?  Eutherian(placental) and non-eutherian mammals diverged 130 million years ago with monotreme mammals diverged 30 million years before marsupials. So does this mean that X inactivation centre reconstituted in eutherian mammals was independently fused in marsupials and monotreme? This finding though leaves us pondering  about the mechanism and evolution of the epigenetic system confirms one thing ,nature not only likes playing fair but also mysterious...
Lynnmaria Nazareth
42259273

Does the Methylated DNA regions in you equals mean of your mom and dad? Yes, No – come on let’s know about it!

Overall opinion is that monozygotic twins are genetically identical and have no differences in any mechanisms, but studies have demonstrated that a monozygotic twin shows differences at the level of DNA methylation. DNA methylation an epigenetic mechanism plays a major role in the developmental regulation of gene expression. DNA methylation is known to contribute to interindividual phenotypic variations which lead to onset of few diseases. These variations are inherited across generations. Across the majority of the genome, DNA methylation is assumed to be complementary on both alleles, although there are several instances where it can be allele-specific.
Inbred mice are ideally suited to study the inheritance of an epigenetic mark like DNA methylation, because the sameness of genetic backgrounds within a strain allows for reproducible mating conditions between two inbred mouse strains. According to the above statements, when two DNA methylated inbred mice are mated, the F1 hybrid should contain methylated DNA regions from both maternal and paternal. The proportions of methylated regions in the F1 hybrid lead to an interesting concept. Let’s find the secret story...!

Refrences:-
Schilling, E., C. El Chartouni, et al. (2009). "Allele-specific DNA methylation in mouse strains is mainly determined by cis-acting sequences." Genome Research 19(11): 2028-2035.

Saranya Srinivasan
42234328

Functional genomic approach to identify novel genes involved in the regulation of oxidative stress resistance and animal lifespan.

Reducing Reactive Oxygen Species (ROS) production can extend animal lifespan by silencing mitochondrial genes through RNAi mediated. Lower ATP levels may activate genes that regulate worm lifespan. Insulin/IGF-1 receptor-like molecule is supposed to double animal lifespan and genes such as daf-2 encoding this molecule when mutated in Caenorhabtidis elegans can also extend its lifespan.

The authors optimized an assay to monitor ROS resistance in worms using the ROS- generating chemical paraquat. Eighty four genes were identified from chromosomes III and IV by developing a functional genomic RNAi screen. The experiment included C. elegans being cultured in a medium containing bacteria expressing interfering dsRNA for the target gene. The worm was reared until L4 stage and a comparison was made between a culture chemically treated with paraquat and another one non- treated. The species strain was rrf- 3 (pk1426), Polymerase Chain Reaction fragment was cloned in the L4440 vector and primers corresponding to a genomic region in daf- 2 and daf- 18 were obtained.

The study found that mutations in daf2 and daf18 can alter sensitivity toward paraquat toxicity. Moreover a screening method for identification of genes involved in regulation of animal lifespan has been created.

Reference: Yongsoon K,Hong S Functional genomic approach to identify novel genes involved in the regulation of oxidative stress resistance and animal lifespan. (2007) Aging Cell 6, pp 489-503 DOI: 10.1111/J. 1474-9726.2007.00302.x.

Patricia Lemos

New discovery about liver cancer cells: SP1 is an essential aspect for activation and chromatin availability of CD151 promoter

Liver cancer is one of the most common malignant neoplastic diseases today. CD151 gene was known as an influential factor of this cancer’s metastasis. It means that ability to detect liver cancer in diagnostics will be more difficult if the level of CD151 is high. Besides, specific protein 1(SP1) plays activating aspect role in transcription.

By using chromatin accessibility analysis in real-time PCR, Wang and colleagues discovered that there was an open chromatin structure lied in the transcription starting site region of CD151 gene. Before being transferred into HepG2 and Hep3B cells, some fragments in the 5’end of CD151 gene were cut and then it was bound with luciferase reporter gene. They found that SP1 was linked with promoter’s core by manipulating electrophoretic mobility shift assay as well as chromatin immunoprecipitation assay. Their research’s result also showed that the CD151 promoter will completely lost its activity when SP1 was removed.

NGUYEN Thi Thu Hang
41882601

Read more at:
http://www.sciencedirect.com.ezproxy.library.uq.edu.au/science?_ob=ArticleURL&_udi=B6WBK-4YC1K0V-1&_user=331728&_coverDate=03%2F05%2F2010&_rdoc=1&_fmt=high&_orig=search&_sort=d&_docanchor=&view=c&_acct=C000016898&_version=1&_urlVersion=0&_userid=331728&md5=4c38a595bd279357db3b068920c2f4e7

Reversing epigenetics: A potential strategy for treating brain tumor

Recent studies have shown that aberrant epigenetic silencing of anti-tumor genes occurs in various cancers in humans. Foltz et al. have reported two novel tumor suppressor genes namely SDC2 and TMTC1 to be silenced in Glioblastoma multiforme (GBM), the most severe type of brain tumor, by an unusual newly found epigenetic mechanism involving methylation of the histone proteins present in their promoters at their specific tails rather than by the usual epigenetic hypermethylation of the promoter sequences. The expression of these genes was restored in brain tumor cells by inhibiting the methylation process, via silencing of DNA methyl transferases (enzymes that bring about the epigenetic methylation and hence the suppression of these genes) using specific siRNA molecules directed against them. The two genes exhibited growth suppressing anti-cancer effects on brain tumor cells in vitro.

The restoration of expression of epigenetically silenced tumor suppressor genes by inhibiting the methylation of the histone tails in brain tumor cells via the use of specific siRNA molecules targeted against DNA methyl transferases, offers a safe and potential therapeutic strategy to treat brain tumor. Also the epigenetic methylation pattern of these specific genes in the glial cells of the brain and their eventual silencing can be used as a marker for early diagnosis of GBM in patients.

REFERENCE:

Foltz, G., Yoon, J. G., Lee, H., Ryken, T. C., Sibenaller, Z., Ehrich, M., et al. (2009). DNA methyltransferase-mediated transcriptional silencing in malignant glioma: a combined whole-genome microarray and promoter array analysis. Oncogene, 28(29), 2667-2677.


Awais Sharjeel Butt
41971608

Stochastic epigenetic variation as a driving force of development, evolutionary adaptation, and disease

Darwin's theory of evolution is based on the natural selection of genetic variations caused by random mutations. On the other hand, Lamarck suggested that phenotypes are shaped by nature and each individual striving to improve for survival. This paper proposes an alternative theory for evolutionary adaptation based on epigenetics. Epigenetic variations, such as varying DNA methylation patterns, that do not modify the phenotype could nevertheless affect its variability and that increased variability may in turn improve fitness and be passed on. The paper provides two experimental results to support their claims. Firstly, the variations in the extent of DNA methylation in the brain constitute evidence in support of stochastic or random epigenetic variation. Secondly, the loss or gain of CpG dinucleotides over time suggests a transmissible genetic mechanism for DNA methylation.


Christophe Boulay


Feinberg, A. P. and R. A. Irizarry (2010). "Stochastic epigenetic variation as a driving force of development, evolutionary adaptation, and disease." Proceedings of the National Academy of Sciences of the United States of America 107: 1757-1764.

Mechanisms of epigenetic silencing of the Rassf1a gene during oestrogen-induced breast carcinogenesis in ACI rats

Epigenetic changes include alterations of chromatin structure mediated by methylation of cytosine residues in CpG dinucleotides, modification of histones by acetylation or methylation, or changes in higher-order chromosome structure. This phenomenon can be found in many tumouigenesis, including breast cancer.

Starland-Davenport demonstrated that oestrogen-induced breast cancer in rats is associated with an aberrant DNA methylation and increase in trimethylation of histone H3 at Rassf1a promoter. In this study, significant increase of 5-methyl-2’-deoxycytidine content in Rassf1a gene was recorded after 12 weeks of oestrogen exposure, whereas other promoter regions, such as, p16, Socs1, Cx26, and Cdh1, which are usually hypermethylated in human breast cancer, did not show any statistically meaningful increase of methylation level. Moreover, complete loss of Rassf1a protein and significant decrease of Socs1 protein was recorded, which suggested that epigenetic modification of these genes are associated with compromised expression of those genes. Aside from that, the substantial increase of H3K9me3 and H3K27me3 (trimethylation of histone H3 lysine 9 and 27) was registered at the promoter regions of Rassf1a and Socs1 genes. This suggests that trimethylation of histones can contribute to the oncogenesis of oestrogen-induced breast cancer.

Even though breast cancer is generally recognised as the alteration of BRCA1 and BRCA2 gene, this study revealed that there is a close correlation between epigenetic modification of Rassf1a and oestrogen-induced breast cancer in rat model.

Original research paper from; Starlard-Davenport, A., et al., Mechanisms of epigenetic silencing of the Rassf1a gene during estrogen-induced breast carcinogenesis in ACI rats. Carcinogenesis, 2010. 31(3): p. 376-381.


Beomjun Kim

Honeybees Show You Are What You Eat

Scientists have made an interesting new discovery in epigenetics, using honeybees.  When honeybees produce female larvae, these larvae are mostly destined to become workers of the colony, but a few however will grow up to become queens.  Queen bees differ significantly from workers in morphological and physiological traits.  Amongst other differences queens are bigger, their reproductive capabilities are massively greater, they behave differently and they live significantly longer.  Where things start to get really interesting though is that genetically identical female larvae can develop into either a worker or a queen depending on what they are fed.

Larvae destined to become queens are fed a substance called royal-jelly by nurse bees, and this is believed to be the causative agent behind whether a bee develops as a worker or a queen.  Kucharski et al (2008) by injecting small interfering RNA into newly hatched bee larvae, were able to silence the expression of DNA methyltransferase Dnmt3 in the larvae.  Dnmt3 is a key component of DNA methylation and epigenetic control in a range of organisms, and by silencing its expression in the bee larvae they caused the larvae to develope in a manner very similar to as if they had been fed royal-jelly.

These results suggest DNA methylation is used to store epigenetic information in honeybees, that this information can be used in different ways depending on nutrition, and that epigenetic modifications can have profound effects on the developmental fate, behavior, size, reproductive capability and longevity of an organism.

Kucharski, R., Maleszka, J., Foret, R., & Maleszka, R.  Nutritional control of reproductive status in honeybees via DNA methylation. Science, 319, 1827-1830.

Jason Raguse (33710727)

Pregnant Mothers: Folate intake may be beneficial for fetal growth, but can also cause asthmatic complications

Every year, 300 million people are affected with asthma, and the numbers continue to increase. New studies have hypothesized that pregnant mothers taking dietary supplements with folate during the early stages of pregnancy may enhance allergic airways disease in their newborn infants.

Diet supplements rich in folate, are important in protecting the growing fetus from developing facial clefting as well as neural tube and cardiac defects. However, it also contains methyl donors which may affect the expression of transcription factors that control lineage of Th1, Th2 and Treg cells, altering DNA methylation, and affecting genetic expression. This in turn results in the increase risk of a child developing allergic airway disease later on in life.

Scientists have tested out this hypothesis with the use of mice, with both dams and pups exposed to different levels of methyl donor diets. Results have indicated that pups that are fed high-methyl donor diet (HMD) or low-methyl donor diet (LMD) have no significant difference, but dams fed with HMD in utero showed higher signs of their pups developing allergic airway disease. Thus, showing that the period of vulnerability of the fetus is during the gestation period.

With that being said, mothers can be forewarned that taking too much folate supplements during the early stages of pregnancy could put a damper on their child's well being.

Source: Hollingsworth, J, Maruoka, S, Boon,K, Garantziotis, S, Li, Z, Tomfohr, J, Bailey, N, Potts, E, Whitehead, G, Brass, D, and Schwartz, D 2008, 'In utero supplementation with methyl donors enhances allergic airway disease in mice.' Journal of Clinical Investigation. Vol. 118, pp. 3462-3469.

Pei - Yi Yap
42238867

Junk DNA – required for a beautiful mind

If you’ve seen the 2002 Best Picture, A Beautiful Mind, starring Russell Crowe, then you’ll know that “junk DNA” – non-protein related products of the central dogma – are definitely worth examining.

Schizophrenia is a severe and complex neural disorder, and one whose cause and pathology is poorly understood. In the past decade, experimental evidence has strongly implicated the importance of microRNAs (miRNAs – small RNA strands that regulate gene expression) , a type of “junk DNA”, in neural development, function and plasticity.

Kocerha et al. (2009) considered the link between miRNAs and schizophrenia. Previous studies had evidenced decreased NMDA (N-methyl-D-aspartate) glutamate receptor signaling – a neurotransmitter – in neural disorders like schizophrenia. Using a mouse model, they investigated the effect of miRNA expression on the NMDA receptor. Their study showed that the expression of a particular miRNA – miR-219 – is involved in neural disorders that are linked to downregulation of the NMDA receptor.

So, it seems that even “junk” is important for a beautiful mind.

Juliana Ip
42265416

Original article:
Kocerha, J., Faghigik, MA., Lopez-Toledano, MA., Huang, J., Ramsey, AJ., Caron, MG., et al. (2009). MicroRNA-219 modulates NMDA receptor-mediated neurobehavioral dysfunction. PNAS – Proceedings of the National Academy of Sciences of the United States of America, 106 (9): 3507-3512

How Wolbachia bateria feminize its male host?

A sex - changing bacteria can change the sex ratios towards females in offspring born by the infected mother hosts, according to a research of Ilaria Negri, Alberto Alma and their teamers.
A team of researchers from three different Italian universities (Turin, Modena and Milan University) corporately unraveled the ability of the bacteria Wolbachia pipientis in reprogramming the male imprinting in its hosts, the leafhoppers Zyginidia pullula, to increase the rate of infected females in the next generation. Wolbachia pipientis is a trans-generational symbiotic parasite that spreads its infection to the next progeny via the hosts' eggs.
Exception of original structure of the last abdominal segment that is still remained in the feminized males; the bacteria altered the males' characteristics so perfectly that they can become females in the observation of genital structure, sexual mates and even productive ability in some cases.
The teams also discovered there were two kinds of feminized males depending on their testes or ovaries found. However, the feminization only occurred with a threshold of bacterial density.
As an external factor of the leafhopper, Wolbachia can prove that changes regarding environmental factors can be inherited from generation to generation. So, which is your side in evolutionary theory- Lamarck or Darwin?

http://rspb.royalsocietypublishing.org/content/early/2009/04/01/rspb.2009.0324.abstract

Thao Tran

Tiny player join transcription initiation

  In a decade, small non-protein coding RNAs - snoRNAs, miRNAs, siRNAs, piRNAs - have been spotlighted as regulators of gene expression at many pathway and tissues. Each class of small RNAs is classified by specific size, biogenesis, and mechanism, and plays a pivotal role in a wide range of biochemical processes beyond the strong bias that introns are just evolutionary debris. Recently, Taft group suggested a novel class of small RNA which may be common characteristics of the transcription initiation, and therefore named as ‘Transcription initiation RNAs (tiRNAs)’

  In the analysis of human, chicken and drosophila RNA sequences, the length of tiRNAs ranged 12-29 nucleotides, which is relatively shorter than any other classes of small RNAs, and in the collaboration with FANTOM 4 project the modal size of them was identified as 18 nucleotides. Remarkably, tiRNAs map to translation start sites (-60 to +120 nucleotides) and are originated from the same strand with TSSs. Moreover, the association with high G+C promoters and major distribution at downstream of TSSs were also found. Inferring from above evidences, Taft groups proposed that tiRNAs may be the result of RNAPII backtracking and stalling.

Joon Yong An

(42057505)

For more read, http://www.nature.com/ng/journal/v41/n5/full/ng.312.html