Prior to the study, it was understood that tRNA's have a specific anti-codon sequence which would recognize a single mRNA codon with the complementary sequence. Does this mean that the tRNA also attaches to different amino acids as well? How does the tRNA differentiate between the different amino acids it is at that moment carrying and the codon it matches with on the mRNA--does it change shape according to which amino acid is attached to it?
activity of the bacterial and eukaryal enzymes is different, which explains why the genomes and the gene composition of bacteria, eukarya, and archaea have diverged
relation between genome structure and the speed of protein synthesis from its genes
greater the abundance of a protein in a cell the higher the number of triplets found in its gene sequence that can be read by modified tRNAs
biotechnology as the discovery of the relevance of these modifications will allow an improvement in the industrial production of proteins
another parameter with which to optimize the synthesis of proteins from a gene
human insulin is "manufactured" in bacteria and our discovery would allow this production to be increased if we take into account the activity of these enzymes
relevant for the study of cancer: "it is possible that these modification enzymes are over-represented in some kinds of cancer. In fact, this would be logical because cancer cells are highly efficient in producing proteins."
demonstrates how organisms have evolved in a different manner to achieve better adaptations and to have optimum protein translation efficiency
don't exactly know why these enzymes appear or why they are different in bacteria and in eukaryotes but it's clear that they contribute to the separation of genomes of these two groups
genetic code is the same
what has changed is the relative importance of different codons of the code
A recent study uncovers the reasons for the divergent evolution of the genomes of different species. The findings provide information about tRNA modifications which may prove useful in the field of biotechnology, specifically in the industrial production of proteins
DNA methylation is a chemical process where a methyl group is added on either the cytosine ring or the adenine ring, used in "higher leveled" organisms. Important in cell differentiation since methylation will cause cells to "remember" and remain differenciated instead of expressing other genes.
Epigenetics is defined as modifications of the genome, heritable during
cell division, that do not involve a change in the DNA sequence.
Epigenetic alterations in cancer include global hypomethylation
the promoters of housekeeping genes
that are generally protected from methylation.
may lead to aberrant silencing of tumor suppressor genes
discovered loss of imprinting (LOI) in
cancer
Genomic imprinting, the subject of the report by
Nakagawa et al. (2), is an epigenetic modification of a
specific parental allele of a gene, or the chromosome on which it
resides, in the gamete or zygote, leading to differential expression of
the two alleles of the gene in somatic cells of the offspring.
we found that LOI can occur in the normal
colonic mucosa of colorectal cancer patients with LOI in their tumors
This LOI was linked to cases showing
microsatellite instability (MSI) in the tumors
However, these patients
do not have mutations in mismatch repair genes
One potential
cause of MSI in these sporadic cancers is hypermethylatiOn and
epigenetic silencing of the hMLH1 mismatch repair gene
Nakagawa et al. (2) now confirm the original study of Cui
et al. that LOI occurs in both tumor and normal tissue of
patients
The present study (2) also offers an intriguing mechanistic
hypothesis to explain the relationship between H19 DMR
methylation and LOI in these patients
Nevertheless, the study calls attention
to this remarkable highly conserved multifunctional protein,
The potential link to CTCF suggested by this study also calls our
attention to the link among DNA methylation, epigenetics, and
chromatin.
A clue to the link between MSI and epigenetics may be provided by
another sometimes overlooked common thread in epigenetics, namely DNA
replication
repeat-induced gene silencing is thought to
be propagated through hemimethylated intermediates during DNA
replication
The studies of Cui et al. (11), Nishihara et
al. (20), and Nakagawa et al. (2) suggest a new and
provocative view of the timing of epigenetic changes in cancer.
Studies of transgenic mice with
constitutive biallelic expression of IGF2, comparable to
LOI, show reduced apoptosis and increased tumor formation
I conclude by noting that the distinction between cancer genetics
and epigenetics has blurred considerably in recent years
Many
conventional “genetic” mechanisms directly affect proteins that
regulate chromatin,
gene therapy to treat blindness in 12 adults and children with Leber's congenital amaurosis (LCA), a rare inherited eye disease that destroys vision by killing photoreceptors—light-sensitive cells in the retina at the back of the eye.
genetic mutations in retinal cells. one mutated gene that causes the disorder is named RPE65. An enzyme encoded by RPE65 helps break down a derivative of vitamin A called retinol into a substance that photoreceptors need to detect light and send signals to the brain.
injected a harmless virus carrying normal copies of RPE65
proved so much they no longer met the criteria for legal blindness
injected the functional genes into the previously untreated eye
improved as soon as two weeks after the operation: They could navigate an obstacle course, even in dim light, avoiding objects that had tripped them up before, as well as recognize people's faces and read large signs
brains were much more responsive to optical input as well.
second round of gene therapy further strengthened the brain's response to the initially treated eye as well as the newly treated one
that neuroplasticity plays a role
visual cortex responding to the newly flowing channel of information from the second eye bolster activity in areas of the visual cortex responding to the initially treated eye.
John Rinn (RNA researcher at Harvard Medical School) continues on his ongoing research about Long Intergenic Noncoding RNA's (lincRNAs). lincRNAs used to be overlooked and classified as 'waste' products, but today it is seen as the contractors that create the DNA's coding sequence needed for the organism's structure. In simpler terms, lincRNAs are responsible for putting molecular materials in places they are supposed to be - as though following a rough draft to make a final master piece. Because lincRNAs have so many functions, if step goes wrong, it could cause potential harm to the organism such as creating a tumor. But because of their many functions like guiding the interactions of protein DNA to name one, John Rinn and other current scientists hypothesize that lincRNAs are what differentiates us from other organisms and makes us, us.
Researchers in IMIM have discovered the function of the enzyme LOXL2, which is one of the factor causing cancer. The enzyme interacts with histone H3, and changes the DNA sequence around that histone, eliminating the lysine 4 amino acid group, which favors tumor development
Having sex allows us to evolve more effectively than species which reproduce without a partner, according to tests that claim to finally prove the long-held theory.
cording to the study by the University of Edinburgh.
Combining the genes of two parents – rather than one in the case of fruit flies, stick insects and other animals – allows for damaging DNA to be removed within a few generations.
Meanwhile, creatures who reproduce asexually are more likely to be lumbered with disease-causing genes
h longer, a
or muc
This is because individuals who inherit healthy genes tend to flourish and pass on their DNA to the next generatio
researchers have identified a generic approach to correct mutations in human mitochondrial DNA by targeting corrective RNAs,
In adults, many aging disorders have been associated with defects of mitochondrial function, including diabetes, Parkinson’s disease, cancer, heart disease, stroke, and Alzheimer’s disease.
The introduction of nucleus-encoded small RNAs into mitochondria is critical for the replication, transcription, and translation of the mitochondrial genome,
The study defined a new role for a protein called polynucleotide phosphorylase (PNPASE) in regulating the import of RNA into mitochondria. Reducing the expression--or output--of PNPASE decreased RNA import, which impaired the processing of mitochondrial genome-encoded RNAs. Reduced RNA processing inhibited the translation of proteins required to maintain the mitochondrial electron transport chain that consumes oxygen during cell respiration to produce energy. With reduced PNPASE, unprocessed mitochondrial-encoded RNAs accumulated, protein translation was inhibited, and energy production was compromised, leading to stalled cell growth.
Geng Wang developed a strategy to target and import specific RNA molecules encoded in the nucleus into the mitochondria and, once there, to express proteins needed to repair mitochondrial gene mutations.
First, the researchers had to find a way to stabilize the reparative RNA so that it was moved out of the nucleus and then localized to the mitochondrial outer membrane. This was accomplished by modifying an export sequence to direct the RNA to the mitochondrion. once the RNA was in the area of the transport machinery on the mitochondrial surface, then a second transport sequence was required to direct the RNA into the targeted organelle. With these two modifications, a wide range of RNAs were targeted to and imported into the mitochondria, where they worked to repair defects in mitochondrial respiration and energy production in two different cell line models of human mitochondrial disease.
This article shows the importance of the RNAs in making proteins for the mitochondria to work efficiently. The article summarizes a method in repairing the mitochondria that is still being worked on.
According to
BEUC, an overwhelming majority of EU consumers do not want cloning to be used
for food production purposes. Some 84 per cent are concerned about the
long-term health and safety impacts.
hippocampus, normally shrinks with age, but if the process speeds up, it could increase vulnerability to Alzheimer's disease
two genes associated with intracranial volume -- the space within the skull occupied by the brain when the brain is fully developed in a person's lifespan
gene variants identified in the first study do not cause Alzheimer's, but they may rob the hippocampus of a kind of "reserve" against the disease
cause cell destruction and dramatic shrinkage of this key brain site
almost twice the Alzheimer's risk if he or she had these versions of the gene
if a person with one of these variants did get Alzheimer's, the disease would attack an already compromised hippocampus and so would lead to a more severe condition at a younger age than otherwise
Alzheimer's disease causes much of its damage by shrinking hippocampus volume
loses a greater-than-average amount of volume due to the gene variants we've identified, the hippocampus is more vulnerable to Alzheimer's
associations impacting intracranial volume, which is an indirect measure of the size of the brain at full development.
brain volume and intracranial volume are both highly heritable
no associations for brain volume
one of these genes has played a unique evolutionary role in human development, and perhaps we as a species are selecting this gene as a way of providing further advances in brain development
The shrinking of the hippocampus, which occurs with age in normal people, was found to be accelerated by certain versions of four genes, which could increase susceptibility to Alzheimer's disease, which also affects the volume of the hippocampus.
Social stress is known to have adverse health effects on both humans and primates. Now, researchers report that it also affects the immune system of female rhesus macaques at the genetic level.
linked atypical gene activity to excessive growth in the autistic brain
autistic brain sprouts an excess of neurons and continues to balloon during the first five years of life, as all those extra neurons grow larger and form connections.
start to lose neural connections, faster than typical brains
67 percent more neurons in their prefrontal cortex (PFC) than typical children
executive functions"—high-level thinking, such as planning ahead, inhibiting impulses and directing attention.
In brain tissue from both autistic children and autistic adults, genes coding for proteins that identify and repair mistakes in DNA were expressed at unusually low levels. Additionally, all autistic brains demonstrated unusual activity levels for genes that determine when neurons grow and die and how newborn neurons migrate during early development
Some genes involved in immune responses, cell-to-cell communication and tissue repair, however, were expressed at unusual levels in adult autistic brains, but not in autistic children's brains
Errors accumulate.
autistic child develops in the womb, something—an inherited mutation or an environmental factor like a virus, toxin or hormone—muffles the expression of genes coding for proteins that usually fix mistakes in sequences of DNA
The genetic systems controlling the growth of new neurons go haywire, and brain cells divide much more frequently than usual, accounting for the excess neurons found in the PFC of autistic children.
autistic brain grow physically larger and form more connections than in a typical child's brain.
immune system reacts against the brain's overzealous growth,
Not all researchers, however, accept
If scientists definitively link autism to a characteristic sequence of changes in gene expression and unusual neural growth, then it becomes possible to target and reverse any one of the thousands of steps in that sequence.
Cancer epigenetics is hot. At the annual meeting of the American Association for Cancer Research in April, once-obscure principal investigators were feted by gaggles of admirers and many poster presenters mobbed by the curious. "It's one of the hottest areas of basic biology," said Paul Workman, Ph.D., director of cancer therapeutics at Cancer Research U.K.
Chloroplasts, the plant cell's green solar power generators, were once living beings in their own right.
This changed about one billion years ago, when they were swallowed up but not digested by larger cells.
either direct transport in the form of DNA fragments from the chloroplasts to the nucleus or transport in the form of mRNA, which is then transcribed back into DNA.
Genes consist of several modules, separated by non-coding DNA regions (introns).
Since the introns obstruct protein synthesis, they need to be removed from the mRNA, a procedure described as splicing.
t is thought that the introns even help the splicing enzymes by folding themselves into stable RNA structures, thus directing the enzymes to the right locations.
It was found that the transfer takes place without the involvement of RNA and that the DNA apparently jumps directly from the cell's chloroplasts into its nucleus.
Drugs that alter some chemical tags on DNA make cancer cells behave more like normal cells
And the drugs seem to make cancer cells more susceptible to chemotherapy and attacks from the immune system.
drugs called azacitidine and decitabine, when used in low doses, change gene activity in leukemia and breast cancer cells in the lab. If DNA is a cell’s hard drive, then chemical tags attached to the DNA or DNA-packaging proteins called histones serve as software packages to tell the hard drive how to function. This type of chemical programming is called epigenetics.
A recent study examined the interaction between a specific microRNA (miRNA) and the activity of the inflammatory cytokine interleukin 13 (IL-13).
In the current study, investigators at the Cincinnati Children's Hospital Medical Center (Ohio, USA) examined the effect that stimulation of IL-13 activity has on microRNAs, particularly miR-375
They reported in the March 28, 2012, online edition of the journal Mucosal Immunology that IL-13 induced changes in epithelial gene and protein expression including the consistent downregulation of miR-375 in IL-13 stimulated human esophageal squamous and bronchial epithelial cells.
Analysis of miR-375 levels in a human disease characterized by IL-13 overproduction - the allergic disorder eosinophilic esophagitis (EE) - revealed downregulation of miR-375 in EE patient samples compared with control patients. Low levels of miR-375 expression levels indicated disease activity.
“MiR-375 is proof of principle that microRNAs are involved in fine-tuning IL-13-mediated responses, which opens up a set of new possibilities for novel therapeutic targets for treatment of allergic disease.”
“The identification of a microRNA that regulates IL-13-induced changes and inflammatory pathways is a significant advancement for the understanding and future treatment of allergic disease,
This discovery, made by a team of researchers from the University of Michigan (USA) and the University of California, Irvine (USA) and published in the journal Nature January 26, 2011 [Transient Hoogsteen base pairs in canonical duplex DNA] involves a new capability of nuclear magnetic resonance (NMR) machines and something most people have never heard of (including me): Hoogsteen base pairs.
It was discovered by the biologist Karst Hoogsteen in 1963. In effect, the Hoogsteen base pair is a ‘normal’ Watson-Crick base pair (usually A-T) flipped-over like an upside-down step on a ladder.
It changes the geometry and allows for truly exotic formations such as a triple helix or even quadruplex structures.
Hoogsteen base pairs were known to exist primarily in RNA and had been observed in DNA only when there was damage to the DNA structure, or something else like a protein or drug was bound to it.
In RNA the Hoogsteen base pairs have been studied fairly extensively. They are considered an “excited state” and are useful to observe unusual protein binding. In DNA the Hoogsteen base pairing, which by the way has two forms, normal and reverse, was considered an anomaly.
It was discovered that normal DNA undergoes these shifts about 1% of the time and they last only milliseconds.
“Together, these data suggest that there are multiple layers of information stored in the genetic code.”
Because critical interactions between DNA and proteins are thought to be directed by both the sequence of bases and the flexing of the DNA molecule, these excited states represent a whole new level of information contained in the genetic code.