You Don't Deserve It, You Never Did. I Want To Wash Off That Pain And Make It Like It Never Happened.

One day a voice rings out from everywhere at once: “Thank you all for participating in the LIFE beta. The servers will be shutting down and undergo a wipe in preparation for a full release of the game.”

Before we can live in a world of vertical gardens covering stained glass skyscrapers, we need to build a world of backyard garden boxes made of reclaimed wood. Before we can cover every rooftop with solar panels, we need to equip every home with solar smokeless cooking made of scrap metal

The appeal of those green cityscapes in the pretty pictures isn’t just that they’re hi-tech and clean, it’s that they sprout from a society that values compassion, the environment, and human lives more than it values profit. We need to build that society first, and we need to build it from the ground up with what we have available

The solarpunk future is for our grandchildren. Our job is to pave the way for it

Onward, steed!

Mysterious DNA modification seen in stress response

With advances in genomics, scientists are discovering additional components of the DNA alphabet in animals. Do these unusual chemical modifications of DNA have a special meaning, or are they just signs that cellular machines are making mistakes?

Geneticists at Emory University School of Medicine led by Peng Jin, PhD have been studying a modification of DNA that is not well understood in animals: methylation of the DNA letter A (adenine). They’ve found that it appears more in the brain under conditions of stress, and may have a role in neuropsychiatric disorders.

The results were published on Oct. 24 in Nature Communications.

Methylation on the DNA letter C (cytosine) generally shuts genes off and is an important part of epigenetic regulation, a way for cells to change how the DNA code is read without altering the DNA letters themselves. Methylation describes a mark consisting of an extra carbon atom and three hydrogens: -CH3.

What if methylation appears on adenine? In bacteria, N6-methyladenine is part of how they defend themselves against invasion by phages (viruses that infect bacteria). The same modification was recently identified as present in the DNA of insects and mammals, but this epigenetic flourish has been awaiting a full explanation of its function.

Just to start, having that extra -CH3 jutting out of the DNA could get in the way of proteins that bind DNA and direct gene activity. For C-methylation, scientists know a lot about the enzymes that grab it, add it or erase it. For A-methylation, less is known.

“We found that 6-methyl A is dynamic, which could suggest a functional role,” Jin says. “That said, the enzymes that recognize, add and erase this type of DNA methylation are still mysterious.”

It does appear that the enzymes that add methyl groups to A when it is part of RNA are not involved, he adds.

First author Bing Yao, PhD, assistant professor of human genetics, recently established his own laboratory at Emory to examine these and other emerging parts of the DNA alphabet. Jin is vice chair of research in the Department of Human Genetics.

In the Nature Communications paper, Yao, Jin and their colleagues looked at the prefrontal cortex region of the brain in mice that were subjected to stress, in standard models for the study of depression (forced swim test and tail suspension test).

Under these conditions, the abundance of N6-methyladenine in the brain cells’ DNA rose four-fold, the scientists found. The DNA modification was detected with two sensitive techniques: liquid chromatography/mass spectrometry and binding to an antibody against N6-methyladenine. The peak abundance is about 25 parts per million, which isn’t that high - but it appears to be confined to certain regions of the genome.

The methyl-A modification tended to appear more in regions that were between genes and was mostly excluded from the parts of the genome that encode proteins. The loss of methyl-A correlates with genes that are upregulated with stress, suggesting that something removes it around active genes. There does seem to be some “cross talk” between A and C methylation, Jin adds.

Genes bearing stress-induced 6mA changes overlapped with those associated with neuropsychiatric disorders; a relationship that needs more investigation. The scientists speculate that aberrant 6mA in response to stress could contribute to neuropsychiatric diseases by ectopically recruiting DNA binding proteins.

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“My domain is time,” said the Genie. “Instead of three wishes, you get three decisions. Go back and choose again.”

The bassoon causing new brain disorder

Mutations have been found in the bassoon (BSN) gene, which is involved with the central nervous system, in patients with symptoms similar to, but different from, a rare brain disorder called progressive supranuclear palsy (PSP).

PSP, a form of Parkinson’s disease, is often difficult to diagnose because it can affect people in different ways. Serious problems often include difficulty with walking and balance in addition to a decline in cognitive abilities such as frontal lobe dysfunction.

A team of Japanese researchers investigated patients whose symptoms resembled not only PSP but also Alzheimer’s disease. Despite similarities in the symptoms, detailed pathological analyses showed no resemblance to either disease, which prompted the team to further research the new disease’s underlying mechanism.

They first analyzed the genomes of a Japanese family with several members displaying PSP-like symptoms. They identified a mutation in the BSN gene only in family members with symptoms. These individuals did not have mutations in the 52 other genes associated with PSP and other neurological disorders such as Alzheimer’s and Parkinson’s. This was the first time BSN gene is associated with a neurological disorder.

(Image caption: MRI analysis of a patient with PSP-like symptoms showed severe atrophy of the bilateral hippocampus, mesencephalic tegmentum, cerebellum, and brainstem. Credit: Yabe I. et al., Scientific Reports, January 16, 2018)

The researchers also detected three other mutations in the BSN gene in four out of 41 other patients displaying sporadic, or non-familial, PSP-like symptoms. None of the BSN mutations were detected in a random sample of 100 healthy individuals, underscoring the strong involvement of BSN mutations in the disease.

An autopsy done on one of the family members with the BSN mutation showed an accumulation of a protein called tau in the brain, which is not seen in a normal brain. The researchers believe that the BSN mutation is involved in the tau accumulation, which could cause the development of PSP-like symptoms. An experiment introducing a mutated rat BSN gene to cultured cells also suggested that the mutation causes the accumulation of tau. Communication between nerve fibres could also be affected, as BSN protein play a role in it.

(Image caption: Tau proteins accumulated in the brain of a patient with PSP-like symptoms. Credit: Yabe I. et al., Scientific Reports, January 16, 2018)

“This is a peculiar neurodegenerative disorder which involves mutations in the BSN gene and tau accumulation, but differs from any known disease, including dementia, Parkinson’s, and even PSP,” says Associate Professor Ichiro Yabe of Hokkaido University who led the study. “Patients with PSP-like symptoms and other neurodegenerative disorders should be analyzed for BSN mutations to fine-tune their diagnoses.”