Molecular genetic student.
DNA double strand break.
Ionising adiation and reactive oxygen species such as superoxide, hydroxyl can cause DNA double strand break. When this happens, it can cause severe damage. There are two mechanisms which response to this type of DNA damage.
1. Homologous recombination repair. Uses the undamaged sister chromatid .
2. Non homologous end-joining repair. Requires complex of repair protein.
![scinerds:
Geneticists Evolve Fruit Flies With the Ability to Count
A team of geneticists has announced that they have successfully bred fruit flies with the capacity to count.
After repeatedly subjecting fruit flies to a stimulus designed to teach numerical skills, the evolutionary geneticists finally hit on a generation of flies that could count — it took 40 tries before the species’ evolution occurred.
The findings, announced at the First Joint Congress on Evolutionary Biology in Canada, could lead to a better understanding of how we process numbers and the genetics behind dyscalculia — a learning disability that affects a person’s ability to count and do basic arithmetic.
“The obvious next step is to see how [the flies’] neuro-architecture has changed,” said geneticist Tristan Long, of Canada’s Wilfrid Laurier University, who admits far more research is needed to delve into what the results actually mean. Primarily, this will involve comparing the genetic make-up of an evolved fruit fly with that of a standard test fly to pinpoint the mutation.](http://25.media.tumblr.com/tumblr_m72hdb8Br61qbn6nco1_500.jpg)
Geneticists Evolve Fruit Flies With the Ability to Count
A team of geneticists has announced that they have successfully bred fruit flies with the capacity to count.
After repeatedly subjecting fruit flies to a stimulus designed to teach numerical skills, the evolutionary geneticists finally hit on a generation of flies that could count — it took 40 tries before the species’ evolution occurred.
The findings, announced at the First Joint Congress on Evolutionary Biology in Canada, could lead to a better understanding of how we process numbers and the genetics behind dyscalculia — a learning disability that affects a person’s ability to count and do basic arithmetic.
“The obvious next step is to see how [the flies’] neuro-architecture has changed,” said geneticist Tristan Long, of Canada’s Wilfrid Laurier University, who admits far more research is needed to delve into what the results actually mean. Primarily, this will involve comparing the genetic make-up of an evolved fruit fly with that of a standard test fly to pinpoint the mutation.
ScienceDaily (July 2, 2012) — Researchers have identified genetic markers that may influence whether a person finishes high school and goes on to college, according to a national longitudinal study of thousands of young Americans.
The study is in the July issue of Developmental Psychology, a…
Beyond Base-Pairs: Mapping the Functional Genome
Regulatory sequences of mouse genome sequenced for first timePopularly dubbed “the book of life,” the human genome is extraordinarily difficult to read. But without full knowledge of its grammar and syntax, the genome’s 2.9 billion base-pairs of adenine and thymine, cytosine and guanine provide limited insights into humanity’s underlying genetics.
In a paper published in the July 1, 2012 issue of the journal Nature, researchers at the Ludwig Institute for Cancer Research and the University of California, San Diego School of Medicine open the book further, mapping for the first time a significant portion of the functional sequences of the mouse genome, the most widely used mammalian model organism in biomedical research.
“We’ve known the precise alphabet of the human genome for more than a decade, but not necessarily how those letters make meaningful words, paragraphs or life,” said Bing Ren, PhD, head of the Laboratory of Gene Regulation at the Ludwig Institute for Cancer Research at UC San Diego. “We know, for example, that only one to two percent of the functional genome codes for proteins, but that there are highly conserved regions in the genome outside of protein-coding that affect genes and disease development. It’s clear these regions do something or they would have changed or disappeared.”
Chief among those regions are cis-regulatory elements, key stretches of DNA that appear to regulate the transcription of genes. Misregulation of genes can result in diseases like cancer. Using high-throughput sequencing technologies, Ren and colleagues mapped nearly 300,000 mouse cis-regulatory elements in 19 different types of tissue and cell. The unprecedented work provided a functional annotation of nearly 11 percent of the mouse genome, and more than 70 percent of the conserved, non-coding sequences shared with other mammalian species, including humans.
As expected, the researchers identified different sequences that promote or start gene activity, enhance its activity and define where it occurs in the body during development. More surprising, said Ren, was that the structural organization of the cis-regulatory elements are grouped into discrete clusters corresponding to spatial domains. “It’s a case of form following function,” he said. “It makes sense.”
While the research is fundamentally revealing, Ren noted it is also just a beginning, a partial picture of the functional genome. Additional studies will be needed in other types of cells and at different stages of development.
“We’ve mapped and understand 11 percent of the genome,” said Ren. “There’s still a long way to march.”
Male Human Sex Chromosomes X and Y (Pair 23), scanning electron micrograph (SEM). There are 23 pairs of chromosomes in most normal human cells. These are allocated pairs 1 - 22 with pair 23 being the sex chromosomes, either xx for females and xy for males. Magnification x17500 at 10 cm wide.
June 25, 2012
A new study involving children with Williams syndrome (WS) suggests that improved regulation of oxytocin and vasopressin may someday improve care for autism, anxiety, post-traumatic stress disorder and WS.
WS results when certain genes are absent because…
Cancer cell dividing
This was taken by Kuan-Chung Su at our London Research Institute. It’s actually an image of 27 stills of a cancer cell dividing. Our cells divide millions of times a day – understanding this process is key in our fight against cancer. More info on our blog:http://bit.ly/NTx4oN
Credit: Kuan-Chung Su, London Research Institute, Cancer Research UK
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(via scinerds)
Transposition of virus and human evolution
How the origin of mammals could be written in our genome … by viruses.
Every human being starts the same way, with a sperm and egg becoming one, 23 chromosomes from each parent contributing the genetic instructions that will one day make, well … you. But the genes, the actual DNA that writes for proteins, make up only about one one-hundredth of all the DNA in those 46 chromosomes.
A full 8% of the DNA in your genome, though, are the remains of ancient viruses. A certain type of virus called a “retrovirus” is capable of inserting its genome into its host, literally writing itself into your DNA. This is the family that HIV belongs to. If a retrovirus infects an egg and inserts its genome, it can get passed down to the next generation. We are full of these remnants, as inactive but still recognizable fossils of past infections.
Dr. Samuel Pfaff and his team were trying to come up with a list of genes that were turned on in a developing mouse embryo, just after sperm and egg had come together. In its earliest stages, an embryo’s cells can become any tissue (one of the ideas behind stem cell therapies). What genes make this possible?
It turns out that for over 100 genes, the switches (called “promoters”) that turned them on came from a very unlikely place: viruses. WHAT?! We know that these genes must be activated in order for an embryo to correctly develop, but the switches that control them come from ancient viral infections! The genes themselves? Purely mouse.
What an odd paradox of evolution!! We need these genes on at a very precise moment, and off a short while after that. If any of it goes wrong, no baby mouse. So evolution selects these viral sequences to be the control mechanism. Could an ancient infection have been the key to the very existence of mammals?
Carl Zimmer has more at The Loom.
Researchers at the University of California, San Diego School of Medicine have uncovered a new signal transduction pathway specifically devoted to the regulation of alternative RNA splicing, a process that allows a single gene to produce or code multiple types of protein variants. The discovery, published in the June 27, 2012 issue of Molecular Cell, suggests the new pathway might be a fruitful target for new cancer drugs.
Signal transduction in the cell involves kinases and phosphatases, enzymes that transfer or remove phosphates in protein molecules in a cascade or pathway. SRPK kinases, first described by Xiang-Dong Fu, PhD, professor of cellular and molecular medicine at UC San Diego in 1994, are involved in controlling the activities of splicing regulators in mammalian cells.
Prior studies have implicated SRPK1 in cancer and other human diseases. For example, it has been shown that SRPK1 plays a critical role in regulating the function of Vascular Endothelial Growth Factor or VEGF, which stimulates blood vessel growth in cancer. SRPK1 has been found to be dysregulated in a number of cancers, from kidney and breast to lung and pancreatic.
Conversely, studies suggest the absence of SRPK1 may be problematic as well, at least in terms of controlling some specific cancer phenotypes. Reduced SRPK1, for example, has been linked to drug resistance, a major problem in chemotherapy of cancer.
In their new paper, Fu and colleagues place SRPK1 in a major signal transduction pathway in the cell. “The kinase sits right in the middle of the PI3K-Akt pathway to specifically relay the growth signal to regulate alternative splicing in the nucleus,” said Fu. “It’s a new signaling branch that has previously escaped detection.”
As such, the SRPK offers a new target for disease intervention and treatment, researchers say. “It’s a good target because of its central role and because it can be manipulated with compounds that suppress its activity, which appears quite effective in suppressing blood vessel formation in cancer,” Fu said.
Three human epithelial cells that have been triple stained. DNA is in blue.
Image by Dr. Jennifer Waters, Wake Forest University.
(via biocanvas)
