genetics and genomics

anonymous asked:

Do you think that some cabins have demigods with powers that fall in the range of their parent's, but is completely opposite the rest of their half-siblings? Say, an Apollo kid who makes people sicker or a an especially hyperactive Hypnos kid?

Yes! That’s something I fully support, because each reaction has an equal and opposite reaction, meaning for each possible power there is an opposite power, within reason. I think it depends on how the god manifested themselves upon meeting the mortal parent. The Twelve Olympians are gods/goddesses of multiple things, such as Hermes being the god of travelers and thieves. In a very simplified example, if you met Hermes at like a hostel vs if you met him on a heist of some sorts.

I think that in part explains the variance in powers, and how most children would have very similar powers, like a lot of Apollo kids are healers due to their parents meeting Apollo in a situation where he was a doctor or a healer of some sort.

However, that’s just a hypothesis. I’m sure there’s also a variance of randomness in there, because god’s don’t have DNA so there’s no hereditary traits. But, that brings up the question of how demigods get any traits from the parents like all Hermes kids having the same mischievous look annnnd now I’m getting off topic and geeking out over genetics.

But yeah, I totally support polar-opposite demigod powers.

nature.com
Gene-edited 'micropigs' to be sold as pets at Chinese institute
Cutting-edge gene-editing techniques have produced an unexpected byproduct — tiny pigs that a leading Chinese genomics institute will soon sell as pets. The pigs are endearing but scientists warn that they may be a distraction from more serious research.
nature.com
Octopus genome holds clues to uncanny intelligence
DNA sequence expanded in areas otherwise reserved for vertebrates.

With its eight prehensile arms lined with suckers, camera-like eyes, elaborate repertoire of camouflage tricks and spooky intelligence, the octopus is like no other creature on Earth.

Added to those distinctions is an unusually large genome, described in Nature1 on 12 August, that helps to explain how a mere mollusc evolved into an otherworldly being.

“It’s the first sequenced genome from something like an alien,” jokes neurobiologist Clifton Ragsdale of the University of Chicago in Illinois, who co-led the genetic analysis of the California two-spot octopus (Octopus bimaculoides).

The work was carried out by researchers from the University of Chicago, the University of California, Berkeley, the University of Heidelberg in Germany and the Okinawa Institute of Science and Technology in Japan. The scientists also investigated gene expression in twelve different types of octopus tissue.

“It’s important for us to know the genome, because it gives us insights into how the sophisticated cognitive skills of octopuses evolved,” says neurobiologist Benny Hochner at the Hebrew University of Jerusalem in Israel, who has studied octopus neurophysiology for 20 years. Researchers want to understand how the cephalopods, a class of free-floating molluscs, produced a creature that is clever enough to navigate highly complex mazes and open jars filled with tasty crabs.

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Seeking SciNote, Biology: CRISPR

Question:

What do geneticists think will be possible when the the new gene-splicing CRISPR is fully operational on patients?

Answer:

For those of us unfamiliar, CRISPR is a revolutionary new genetic splicing technology. Gene splicing refers to modifications to a gene transcript that can result in different proteins being made from a single gene. Interestingly, CRISPR’s inception began when dairy scientists discovered that bacteria used to create yogurt (by transforming lactose into lactic acid) had incorporated snippets of benign viruses into its genome. To their surprise, the incorporated DNA would create toxic agents to thwart infective viruses. In 2007, dairy scientists realized that they could effectively fortify bacteria by adding spacer DNA, which does not code for any protein sequence, from a virus. Then, five years later, as Time Magazine writer Alice Park skilfully describes, professors Jennifer Doudna and Emanuelle Charpentier noticed “up to 40% of bacteria developed a particular genetic pattern in their genomes. What they found were sequences of genes immediately followed by the same sequence in reverse, known as palindromic sequences. Further, bits of random DNA bases cropped up after each such pairing and right before the next one. After the dairy bacteria transcribed its spacer DNA and palindromic sequence into RNA, it self-spliced those segments into shorter fragments, with an enzyme called CAS9”. As you may be wondering, CRISPR stands for “clustered regularly interspaced short palindromic repeats”.

It is important for us to emphasize the versatility of this method. In the 2007 article, Doudna and Charpentier go into depth regarding the many benefits of the new genetic technology. These include the potential to “systematically analyze gene functions in mammalian cells, study genomic rearrangements and the progression of cancers or other diseases, and potentially correct genetic mutations responsible for inherited disorders”. As you might imagine, this opens up possibilities that were previously science fiction. Currently, painful blood transfusions are commonplace in the treatment of many diseases such as sickle cell anemia. Sickle cell affects red blood cells, which are made by stem cells in bone marrow. Soon, Massachusetts Institute of Technology synthetic biologist Feng Zhang envisions that this will soon no longer be necessary. She predicts that after doctors extract some of the marrow, scientists will splice out the defective fragment of DNA using CRISPR from the removed stem cells, then bathe the cells in a solution containing the non-sickle-cell sequence. As the DNA repairs itself naturally, it picks up the correct sequence and incorporates it into the stem cell genomes. After this one-time procedure, the stem cells would give rise to more red blood cells with the healthy gene. Eventually, the blood system would be repopulated with normal cells.


The treatment of HIV using CRISPR would be very similar. In this potential treatment, “patients would provide a sample of blood stem cells from their bone marrow, which would be treated with CRISPR to remove the CCR5 gene, and these cells would be transplanted back to the patient. Since the bone marrow stem cells populate the entire blood and immune system, the patient would eventually have blood cells that were protected, or “immunized,” against HIV”.


Despite this extraordinary potential, no biological technology comes without serious ethical concerns. As Jennifer Douda says herself, CRISPR “really requires us to careful thought to how we employ such a tool: What are we trying to do with it, what are the appropriate applications, how can we use it safely?”

Check out her book The Stem Cell Hope for learning about the future of stem cell technology.

Sources:
Park, Alice. “A New Gene-Splicing Technique.” 100 New Scientific Discoveries: Fascinating, Unbelievable and Mind-expanding Stories. New York, NY: TIME, 2014. 92-95. Print.

Park, Alice. “It May Be Possible To Prevent HIV Even Without a Vaccine.” Time. Time, 6 Nov. 2014. Web.

Doudna, Jennifer A., and Charpentier, Emmanuelle (2014). The new frontier of genome engineering with CRISPR-Cas9. Science, 346(6213), 1258096–1258096. doi:10.1126/science.1258096

Answered by: Teodora S., Expert Leader and Expert John M.

Edited by: Carrie K.

“I’m fascinated by the idea that genetics is digital. A gene is a long sequence of coded letters, like computer information. Modern biology is becoming very much a branch of information technology.”
 ― Richard Dawkins

youtube

So uh

Last night I 

Kind of got a little drunk

And made this

Oops… 

‘Platinum’ genome takes on disease

Geneticists have a dirty little secret. More than a decade after the official completion of the Human Genome Project, and despite the publication of multiple updates, the sequence still has hundreds of gaps — many in regions linked to disease. Now, several research efforts are closing in on a truly complete human genome sequence, called the platinum genome.

“It’s like mapping Europe and somebody says, ‘Oh, there’s Norway. I really don’t want to have to do the fjords’,” says Ewan Birney, a computational biologist at the European Bioinformatics Institute near Cambridge, UK, who was involved in the Human Genome Project. “Now somebody’s in there and mapping the fjords.”

The efforts, which rely on the DNA from peculiar cellular growths, are uncovering DNA sequences not found in the official human genome sequence that have potential links to conditions such as autism and the neuro-degenerative disease amyotrophic lateral sclerosis (ALS).

In 2000, then US President Bill Clinton joined leading scientists to unveil a draft human genome. Three years later, the project was declared finished. But there were caveats: that human ‘reference’ genome was more than 99% complete, but researchers could not get to 100% because of method limitations.

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anonymous asked:

Fav ones that are still alive and/or working?

Cool women of science that are still alive:

Jocelyn Bell Burnell - Astrophysicist; Discovered radio pulsars (her advisor won the Nobel prize for this). Has been the President of the Royal Astronomical Society, The Institute of Physics, Royal Society of Edinburgh and elected Pro-Chancellor of the University of Dublin.

Elizabeth Blackburn - Molecular Biologist; She co-discovered telomerase the enzyme associated with the repair of telomeres (part of chromosomes). Won the Nobel prize in Medicine in 2009 for this research. On January 1st, 2016 she will become the president of the Salk Institute for Biological Studies.

Shirley Ann Jackson - Physicist; the first African American to earn a doctorate at MIT. She’s the current president of the Rensselaer Polytechnic Institute and has many awards and accomplishments.

Christiane Nüsslein-Volhard - Biologist; won the Nobel Prize in Medicine for the genetics of embryonic development.

Vera Rubin - Astronomer; who did pioneering work on the rotation of galaxies. This work formed the foundation of the current study of Dark Matter.

Mae Jemison - Physician and NASA Astronaut; First African American to travel in space; also practiced medicine in the Peace Corps.

Melissa Franklin - Experimental Particle Physicist; Her team found some of the first evidence for the existence of the top quark.

Darleane C. Hoffman - Nuclear Chemist; was part of a team that confirmed the existence of the element Seaborgium.

Ingrid Daubechies - Mathematician, and the first women to serve as the president of the International Mathematical Union. Her research is on wavelets in image compression.

Sylvia Earle - Marine Biologist; The first female chief scientist of the U.S. National Oceanic and Atmospheric Administration

Mary-Claire King - Geneticist; is known for identifying breast cancer genes, demonstrating that humans and chimpanzees are 99% genetically identical, and using genomic sequencing to identify victims of human rights abuses.

Susan Solomon - Atmospheric Chemist; She and her team proposed the chloroflurocarbon free radical reaction mechanism, which explains the hole in the ozone layer.

Mildred Dresselhaus - Physicist nicknamed the “Queen of Carbon Science; MIT’s first female institute professor and has won many international scientific awards. Known mostly for her work on Carbon nanotubes.

Shirley M. Tilghman - A leader in the field of molecular biology and was Princeton University’s first female president.

Lene Hau - Physicist; She led a scientific team that was able to slow, and then stop the motion of light. Also has done very important work in quantum physics.

Scientists Uncover Common Cell Signaling Pathway Awry in Some Types of Autism

Brain cells grow faster in children with some forms of autism due to distinct changes in core cell signaling patterns, according to research from the laboratory of Anthony Wynshaw-Boris, MD, PhD, chair of the department of genetics and genome sciences at Case Western Reserve University School of Medicine, and a member of the Case Comprehensive Cancer Center. Rapid cell growth can cause early brain overgrowth, a common feature in 20-30% of autistic children. But, the genetics of autistic children vary making it difficult to pinpoint common mechanisms underlying the disease.

“Autism is a complex disorder with multiple genetic and non-genetic factors,” explained Wynshaw-Boris. “Because the causes are diverse, it may help to define a subset of patients that have a common [symptom], in this case early brain overgrowth.”

In a study published in Molecular Psychiatry, Wynshaw-Boris and his colleagues started with skin cell samples from autistic children with enlarged brains and worked backward. Researchers in the laboratory “reprogrammed” donated skin cells to produce cells found in the developing brain including induced pluripotent stem cells and neural progenitor cells. Stem and progenitor cells are important therapeutic tools as they have the potential to grow into a multitude of cell types. The researchers hypothesized that even though the children in the study had different forms of autism, the precursor cells could be used to find common molecular and cellular mechanisms.

The researchers discovered that cells derived from autistic donors grew faster than those from control subjects and activated their genes in distinct patterns. Genes related to cell growth were unusually active, leading to more cells but fewer connections between them. This can cause faulty cell networks unable to properly transmit signals in the brain and enlarged heads during early development.

The researchers identified abnormal genes in the cells grown from autistic donors as belonging to the Wnt signaling pathway. The Wnt genes are critical for cell growth and serve as central players in cell networks, interfacing with multiple signaling pathways. Wynshaw-Boris previously identified the Wnt pathway as related to autism in mouse models of the disease. In a separate study published in Molecular Psychiatry earlier this year, the Wynshaw-Boris laboratory showed mice lacking Wnt genes display autism-like symptoms including social anxiety and repetitive behavior. The researchers could prevent these adult symptoms by treating the mice with medications that activate Wnt signaling in the uterus, during development.

“The Wnt pathway is one of the core developmental pathways conserved from invertebrates to humans. Our studies solidify previous suggestions that this pathway has a role in autism,” said Wynshaw-Boris.

Once they identified the dysfunctional signaling pathway in their reprogrammed autistic samples, the researchers (including the laboratories of Alysson Muotri, PhD at the University of California San Diego and Fred Gage, PhD at the Salk Institute) attempted to correct it by exposing mature nerve cells derived from autistic donors to drug compounds. One drug currently being tested in clinical trials for autism is insulin growth factor 1 (IGF-1). When the researchers added IGF-1 to nerve cells derived from autistic donors, neural networks were reestablished. It is unclear whether the positive effects of IGF-1 were on the Wnt pathway, and the exact compensatory mechanism requires further investigation.

Wynshaw-Boris’s studies in cell culture and mouse models of autism confirm improper Wnt signaling can lead to rapid brain cell growth and brain enlargement in the embryo, resulting in abnormal social behavior after birth. The next step will be to determine which genes are most impacted by Wnt signaling defects during early development, and how these changes result in abnormal behavior. “We would also like to find other drugs or compounds that may slow down the growth of the cells in tissue culture,” said Wynshaw-Boris. Together, these findings may help researchers unravel common ways brain cells can become impaired during early development in carefully chosen subsets of patients and contribute to symptoms across the autism spectrum.

anonymous asked:

I wouldn't bother with that squigglesquo. They are obviously a troll and won't listen anyhow. :/ They're profile is full of them barking orders at strangers they don't have to face.

Yeah. This is the last thing I’ll say to them on this subject. 

squigglesquo, I have a bachelor’s degree in Biology from the University of Notre Dame where I concentrated in Genetics and Genomics, wrote my Honors Senior Thesis on Evolutionary Biology, and composed a Capstone Project on Paleontology. I skipped getting a master’s because I was already qualified enough to join a PhD program. I am now currently a first year grad student at the Molecular Cellular and Developmental Biology PhD program at the University of Illinois at Chicago where I will probably specialize in Evolutionary Developmental Biology. 

So shut. the fuck. up. 

Here are sources that show I am who I say I am. Have fun not clicking them because you’re clearly just a troll. 

(My name is Margaret Dickson and I sometimes go by Meg.)

My high school’s page about me because I was Salutatorian and had a GPA of 98.89% (I also was on the Science Olympiad Team and basically ran our Fossil Event group and got a lot of medals.) 

This is my undergrad lab which doesn’t like to update but my name is on it at least

This is the PDF from a conference I attended and presented my research at

This is the page for the Bio Honors Program at Notre Dame and if you go to the class of 2015 I am there

This is the 2015 graduation science page where another honors program I was in (Glynn Family) mentions me

And here is my graduate program’s page where my name is listed. 


Hey teachers! This summer, enhance your science curriculum from wherever your vacation takes you. The Museum offers online professional development programs, and graduate credit is available. 

The next 6-week session of these courses, Seminars on Science, starts May 25th with online courses including Climate Change; Earth: Inside and Out; Evolution; The Link Between Dinosaurs and Birds; Genetics, Genomics, Genethics; The Ocean System; Sharks and Rays; The Solar System and more.

Enroll by Monday, May 11th. Learn more. 

Drugs stimulate body’s own stem cells to replace the brain cells lost in multiple sclerosis

A pair of topical medicines already alleviating skin conditions each may prove to have another, even more compelling use: instructing stem cells in the brain to reverse damage caused by multiple sclerosis.

Led by researchers at Case Western Reserve, a multi-institutional team used a new discovery approach to identify drugs that could activate mouse and human brain stem cells in the laboratory. The two most potent drugs – one that currently treats athlete’s foot, and the other, eczema – were capable of stimulating the regeneration of damaged brain cells and reversing paralysis when administered systemically to animal models of multiple sclerosis. The results are published online Monday, April 20, in the scientific journal Nature.

“We know that there are stem cells throughout the adult nervous system that are capable of repairing the damage caused by multiple sclerosis, but until now, we had no way to direct them to act,” said Paul Tesar, PhD, the Dr. Donald and Ruth Weber Goodman Professor of Innovative Therapeutics, and associate professor in the Department of Genetics & Genome Sciences at the Case Western Reserve School of Medicine. “Our approach was to find drugs that could catalyze the body’s own stem cells to replace the cells lost in multiple sclerosis.”

The findings mark the most promising developments to date in efforts to help the millions of people around the world who suffer from multiple sclerosis. The disease is the most common chronic neurological disorder among young adults, and results from aberrant immune cells destroying the protective coating, called myelin, around nerve cells in the brain and spinal cord.

Without myelin, neural signals cannot be transmitted properly along nerves; over time, a patient’s ability to walk, hold a cup or even see is inexorably eroded. Current multiple sclerosis therapies aim to slow further myelin destruction by the immune system, but the Case Western Reserve team used a new approach to create new myelin within the nervous system. Their work offers great promise of developing therapies that reverse disabilities caused by multiple sclerosis or similar neurological disorders.

“To replace damaged cells, much of the stem cell field has focused on direct transplantation of stem cell-derived tissues for regenerative medicine, and that approach is likely to provide enormous benefit down the road,” said Tesar, also a New York Stem Cell Foundation Robertson Investigator and member of the National Center for Regenerative Medicine. “But here we asked if we could find a faster and less invasive approach by using drugs to activate native stem cells already in the adult nervous system and direct them to form new myelin. Our ultimate goal was to enhance the body’s ability to repair itself.”

Tesar emphasized that much work remains before multiple sclerosis patients might benefit from the promising approach. Scientists still must find ways to transform the topical medications for internal use and determine their long-term efficacy and potential side effects. That said, using existing, federally approved drugs enhances the likelihood that the compounds can be made safe for human use.

Tesar and his colleagues could zero in on the two catalyzing medications only because of a breakthrough that his laboratory achieved in 2011. Specifically, the researchers developed a unique process to create massive quantities of a special type of stem cell called an oligodendrocyte progenitor cell (OPC). These OPCs are normally found throughout the adult brain and spinal cord, and therefore inaccessible to study. But once Tesar and his team could produce billions of the OPCs with relative ease, they could begin to test different existing drug formulations to determine which, if any, induced the OPCs to form new myelinating cells.

Using a state-of-the-art imaging microscope, the investigators quantified the effects of 727 previously known drugs, all of which have a history of use in patients, on OPCs in the laboratory. The most promising medications fell into two specific chemical classes. From there, the researchers found that miconazole and clobetasol performed best within the respective classes. Miconazole is found in an array of over-the-counter antifungal lotions and powders, including those to treat athlete’s foot. Clobetasol, meanwhile, is typically available by prescription to treat scalp and other skin conditions such as dermatitis. Neither had been previously considered as a therapeutic for multiple sclerosis, but testing revealed each had an ability to stimulate OPCs to form new myelinating cells. When administered systemically to lab mice afflicted with a multiple sclerosis-like disease, both drugs prompted native OPCs to regenerate new myelin.

“It was a striking reversal of disease severity in the mice,” said Robert Miller, PhD, a member of the neurosciences faculty at Case Western Reserve who, with Tesar, is a co-senior author of the Nature paper. The two collaborated on this project while Miller also served as Vice President for Research at Case Western Reserve; since June his primary appointments are at the George Washington University School of Medicine and Health Sciences, where he is Senior Associate Dean for Research and Vivian Gill Distinguished Research Chair. “The drugs that we identified are able to enhance the regenerative capacity of stem cells in the adult nervous system. This truly represents a paradigm shift in how we think about restoring function to multiple sclerosis patients.”

While the drugs proved to have extraordinary effects on mice, their impact on human patients will not be known fully until actual clinical trials. Nevertheless, Tesar and his team already have added reason for optimism; in addition to the tests with animal cells, they also tested the drugs on human stem cells – and saw the medication prompt a similar response as seen in the mouse cells. Both medications worked well, with miconazole demonstrating the more potent effects.

“We have pioneered technologies that enable us to generate both mouse and human OPCs in our laboratory,” said Fadi Najm, MBA, the first author of the study and Research Scientist in the Department of Genetics & Genome Sciences at the Case Western Reserve School of Medicine. “This uniquely positioned us to test if these drugs could also stimulate human OPCs to generate new myelinating cells.”

Tesar, who recently received the 2015 International Society for Stem Cell Research Outstanding Young Investigator Award, said investigators next will work to deepen their understanding of the mechanism by which these drugs act. Once these details are clear, researchers will modify the drugs to increase their effectiveness in people.

The team is enthusiastic that optimized versions of these two drugs can be advanced to clinical testing for multiple sclerosis in the future, but Tesar emphasized the danger of trying to use current versions for systemic human administration.

“We appreciate that some patients or their families feel they cannot wait for the development of specific approved medications,” Tesar said, “but off-label use of the current forms of these drugs is more likely to increase other health concerns than alleviate multiple sclerosis symptoms. We are working tirelessly to ready a safe and effective drug for clinical use.”