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File: 1435022573290.jpg (387.03 KB, 2055x1103, 2055:1103, 1DNA.jpg)

 No.1[Reply]

This board is about specific genes and their effects. Any factors at play may also be discussed.

Studies and Research are encouraged. Hard science in general welcome.

For loose and low moderation discussion there is >>>/speciation/

Anything about races or speciation goes. You can discuss culture, behavior/psychology, and race.

For discussion about races there is >>>/genetics/

Here is a high moderation board that includes epigenetics and general biochemistry.

The difference between /genetics/ and /genes/ is that while genes is specific /genetics/ is broad.

Post last edited at


File: 1458978511520.jpg (137.62 KB, 926x1314, 463:657, 14092877519992966463558910….jpg)

 No.76[Reply]

The CRISPR/Cas9-sgRNA system has been developed to mediate genome editing and become a powerful tool for biological research. Employing the CRISPR/Cas9-sgRNA system for genome editing and manipulation has accelerated research and expanded researchers’ ability to generate genetic models. However, the method evaluating the efficiency of sgRNAs is lacking in plants. Based on the nucleotide compositions and secondary structures of sgRNAs which have been experimentally validated in plants, we instituted criteria to design efficient sgRNAs. To facilitate the assembly of multiple sgRNA cassettes, we also developed a new strategy to rapidly construct CRISPR/Cas9-sgRNA system for multiplex editing in plants. In theory, up to ten single guide RNA (sgRNA) cassettes can be simultaneously assembled into the final binary vectors. As a proof of concept, 21 sgRNAs complying with the criteria were designed and the corresponding Cas9/sgRNAs expression vectors were constructed. Sequencing analysis of transgenic rice plants suggested that 82% of the desired target sites were edited with deletion, insertion, substitution, and inversion, displaying high editing efficiency. This work provides a convenient approach to select efficient sgRNAs for target editing.

The efficient editing of target genes in transgenic plants can provide researcher with desired mutants, which will accelerate the progress of gene function dissection. We confirmed that the sgRNAs complying with the criteria were efficient for target gene editing. Both this work and Ma et al.’s9 confirmed that at least two same snoRNA promoters can be used simultaneously to drive different sgRNAs. Our work also revealed that the number of sgRNA cassettes has no effect on the editing efficiency of sgRNAs. It is noteworthy that up to 84.8% of edited plants contained loss-of-function gene mutations (i.e., biallelic or homozygous mutations) in the T0 transgenic plants and they can be used directly for functional analysis. In our two-sgRNA expression plants, both targets sites can be edited simultaneously, which also caused deletion or inversion of DNA fragment between two target sites. The editing of both target sites will facilitate the gene correction via homologous recombination by providing a mutant plant with wild type DNA fragment donor. Altogether, our toolbox for sgRNA design criteria and assembly of multiplex CRISPR/Cas9-sgRNA systePost too long. Click here to view the full text.



 No.2[Reply]

arrqwertyuiopasdfghjkl;zxcvbnm,qweruiop[asdfghjkqwertyuiowertyuiop1234567890

1234567890-1234567890-=

5 posts omitted. Click reply to view.

 No.64

ra•ce


 No.68

66


 No.71

88


 No.73

11


 No.75

22




File: 1458124687052.jpg (37.18 KB, 400x267, 400:267, 1469579469469.jpg)

 No.74[Reply]

The authors found that enslaved Formica colonies were more genetically and chemically diverse than their free-living counterparts. The researchers think these differences are likely caused by seasonal raids to steal pupa from several adjacent host colonies.

"When free-living Formica ants are kidnapped into the Polyergus colony, they enter a society that [comprises] kidnapped ants from many other Formica colonies. Here, we show that this rich social environment alters the behaviors displayed by the enslaved ants," said Neil Tsutsui.

The different social environments of enslaved and free-living Formica also appear to affect their recognition behaviors: enslaved Formica workers were less aggressive towards non-nest mates than were free-living Formica. Future studies are needed to understand the underlying mechanisms, but the authors suggest their findings indicate that parasitism by P. breviceps alters both the chemical and genetic context in which their hosts develop, leading to changes in how they recognize nest mates.

Our study contrasts with other studies that compared the nestmate recognition systems of monogynous (single queen) with those of polygynous colonies (multiple queens). Martin et al. [71] found that Formica execta colonies with higher genetic diversity (polygynous) had reduced nestmate recognition cue diversity compared to those that were less genetically diverse (monogynous).

https://archive.is/eqPSD

The Effect of Social Parasitism by Polyergus breviceps on the Nestmate Recognition System of Its Host, Formica altipetens



File: 1457045073155.jpg (14.3 KB, 320x132, 80:33, Y2HUH2.jpg)

 No.72[Reply]

Didier Raoult of Aix-Marseille University in France and his colleagues discovered a new kind of virus lurking inside single-celled protozoans back in 2003. Like other viruses, it couldn’t grow on its own, lacking the biochemical machinery to build proteins and genes. Instead, it had to infect host cells and use their material to produce new viruses.

But this new virus was enormous, measuring hundreds of times bigger than any previously known virus. What’s more, it was far more complex. Typical viruses may have just a few genes. The new virus had over 900 — more than many species of bacteria.

Since then, Raoult and his colleagues have found over 150 different kinds of giant viruses all over the world, in oceans, mountains, and the bodies of animals (including our own). One kind of giant virus contains over 2,500 genes.

Exactly what giant viruses do with all those genes has remained mostly a mystery.

But on Monday, Raoult and his colleagues reported in Nature that some of those genes provide giant viruses with something never observed before in a virus: They have an immune system, one that works a lot like the CRISPR system in bacteria that scientists have co-opted as a powerful gene editing tool.

>the potential for such a system to be harnessed for genetic control is intriguing

>Raoult and his colleagues first discovered that giant viruses get infected with viruses of their own back in 2008.

These so-called virophages slip inside the giant viruses and hack their biochemistry, much as the giant viruses do to their own protozoan hosts.

>One of these virophages, called Zamilon, infects a type of giant virus known as a mimivirus. But when Raoult and his colleagues unleashed Zamilon on closely related strains of mimiviruses, they were surprised to find that it couldn’t infect them.

>It appeared as if the giant viruses could defend themselves against their enemies.

Raoult and his colleagues wondered if giant viruses were using a CRISPR-like defense system against Zamilon. To their surprise, they found that Post too long. Click here to view the full text.



File: 1455929003851.jpg (87.24 KB, 923x565, 923:565, 14829247182940274.jpg)

 No.69[Reply]

Beef is banned. Menstruation is taboo. If you think this is today's news, the same made headlines in 1873. The impact of these exhibits however was not long lasting. Caste is not discussed unless it is a matter of life and death, as proven by Rohith Vemula's suicide on January 17. A startling reminder of how the caste system continues to maim and kill, in modern India.

http://archive.is/ev9Kz

India's present diverse population arose from five types of ancient populations that freely mixed and interbred for thousands of years before the rigid caste system, with its principle of prohibition of marriage outside the caste, put an end to this mixing. This ancient history hinted at in various linguistic, archeological and genetic studies has been confirmed by a path-breaking genetic study recently published.

Researchers from the National Institute of Biomedical Genomics (NIBMG) at Kalyani, West Bengal, analysed DNA samples of 367 unrelated Indians belonging to 20 population groups. These covered castes from different parts of India, and most large tribal populations from central and Northeastern India. Also included were samples from two Andaman & Nicobar tribes.

"Genetic analysis shows mainland India's present population is a result of the intermixing of four main types of ancestral populations - North Indian, South Indian, Austro Asian and Tibeto-Burman," said Partha Majumder, director of NIBMG who led the study. The Andaman & Nicobar tribals have a completely different fifth ancestral origin that originated in Pacific Ocean populations.

The study compared genetic sequences from Indian samples with those from Central Asia, West Asia, China and adjacent regions to trace how humans first arrived in India.

What the study also unearthed was the deep imprint of a significant social cultural process in Indian society . It found that interbreeding between communities `abruptly' ended around 70 generations ago, which translates to about 1,575 years ago, sometime in the 6th century .

"To understand this, we lookPost too long. Click here to view the full text.

 No.70




File: 1454583951834.jpg (8.74 KB, 568x346, 284:173, mouse.jpg)

 No.67[Reply]

The Y chromosome is thought to be important for male reproduction. We have previously shown that with the use of assisted reproduction, live offspring can be obtained from mice lacking the entire Y chromosome long arm. Here, we demonstrated that live mouse progeny can also be generated using germ cells from males with the Y chromosome contribution limited to only two genes, the testis determinant factor Sry and the spermatogonial proliferation factor Eif2s3y. Sry is believed to function primarily in sex determination during fetal life. Eif2s3y may be the only Y chromosome gene required to drive mouse spermatogenesis allowing formation of haploid germ cells that are functional in assisted reproduction. Our findings are relevant but not directly translatable to human male infertility cases.

At present, our findings in mice do not translate directly to humans. ROSI is still considered experimental in human ART due to concerns regarding the safety of injecting immature germ cells and technical difficulties (23). In spite of this, some children have already been born (24, 25) and those were healthy. As we learn more about the effects and improve technical aspects of ROSI, this method may become more acceptable. Indeed, studies on ROSI effects in mice have been encouraging (26). Thus our study may bear importance for clinicians working in ART clinics supporting the possibility that ROSI may be a viable option for overcoming infertility in men with non-obstructive azoospermia.

Considering that we have obtained live offspring using germ cells from males with only two Y chromosome genes one could question the importance of Y chromosome in male reproduction. We believe that the answer lies in defining the need. Human Y chromosome is not on the way to oblivion, as it has been implied in the past (27), and its genetic information is undoubtedly important for many aspects of reproduction involving the development of mature sperm and its function in normal fertilization (28). Most of the mouse Y chromosome genes are involved in spermiogenesis and sperm function and as such are necessary for normal fertilization (29, 30). However, when it comes to assisted reproduction, our mouse study proves that the Y chromosome contribution can be brought to a bare minimum consisting of Sry and Eif2s3y. Indeed, it may well be possible to eliminate mouse Y chromosome altoPost too long. Click here to view the full text.



File: 1446090120077.jpg (45.85 KB, 640x353, 640:353, ab77324200d5784f0ccee394f4….jpg)

 No.46[Reply]

Soon enough, a clear picture emerged: the human hippocampus, a brain area critical to learning and memory and often the first region damaged in Alzheimer’s patients, showed evidence of adult neurogenesis. Gage’s collaborators in Sweden were getting the same results. Wanting to be absolutely positive, Gage even sent slides to other labs to analyze. In November 1998, the group published its findings, which were featured on the cover of Nature Medicine.1

“When it came out, it caught the fancy of the public as well as the scientific community,” Gage says. “It had a big impact, because it really confirmed [neurogenesis occurs] in humans.”

Fifteen years later, in 2013, the field got its second (and only other) documentation of new neurons being born in the adult human hippocampus—and this time learned that neurogenesis may continue for most of one’s life.2 Neuroscientist Jonas Frisén of the Karolinksa Institute in Stockholm and his colleagues took advantage of the aboveground nuclear bomb tests carried out by US, UK, and Soviet forces during the Cold War. Atmospheric levels of 14C have been declining at a known rate since such testing was banned in 1963, and Frisén’s group was able to date the birth of neurons in the brains of deceased patients by measuring the amount of 14C in the cells’ DNA.

“What we found was that there was surprisingly much neurogenesis in adult humans,” Frisén says—a level comparable to that of a middle-aged mouse, the species in which the vast majority of adult neurogenesis research is done. “There is hippocampal neurogenesis throughout life in humans.”

But many details remain unclear. How do newly generated neurons in adults influence brain function? Do disruptions to hippocampal neurogenesis play roles in cognitive dysfunction, mood disorders, or even psychosis? Are there ways to increase levels of neurogenesis in humans, and might doing so be therapeutic? Researchers are now seeking to answer these and other questions, while documenting the extent and function of adult neurogenesis in mammals.

https://archive.is/sVwtG

Researchers have also demonstrated that neurogenesis occursPost too long. Click here to view the full text.

 No.54

Sweet


 No.61

>>46

good read




File: 1445494959700.jpg (56.48 KB, 709x522, 709:522, celegansneurons.jpg)

 No.44[Reply]

New Neurons Discovered in C. Elegans

Caenorhabditis elegans worms have two sexes: hermaphrodite and male. Hermaphrodites, the best studied, have just 302 neurons, but males have more — the MCMs raise their total to 385 neurons1.

NHGRIIn a species whose neural circuits have been comprehensively mapped, researchers at University College London and their colleagues have identified a new type of neuron. These glia-derived neurons, which researchers dubbed “mystery cells of the male,” or MCMs, are tied to sex-specific learning in the roundworm Caenorhabditis elegans. Researchers reported their finding in Nature last week (October 14).

Finding a new set of neurons in a well-studied system “is a bit of a shock,” study coauthor Richard Poole of University College London told Nature News, which noted that the team next plans to explore MCMs’ roles in brain sex differences and in learning. (See “Sex Differences in the Brain,” The Scientist, October 2015.)

Sex differences in behaviour extend to cognitive-like processes such as learning, but the underlying dimorphisms in neural circuit development and organization that generate these behavioural differences are largely unknown. Here we define at the single-cell level—from development, through neural circuit connectivity, to function—the neural basis of a sex-specific learning in the nematode Caenorhabditis elegans.

We show that sexual conditioning, a form of associative learning, requires a pair of male-specific interneurons whose progenitors are fully differentiated glia.

These neurons are generated during sexual maturation and incorporated into pre-exisiting sex-shared circuits to couple chemotactic responses to reproductive priorities.

Our findings reveal a general role for glia as neural progenitors across metazoan taxa and demonstrate that the addition of sex-specific neuron types to brain circuits during sexual maturation is an important mechanism for the generation of sexually dimorphic plasticity in learning.

Post too long. Click here to view the full text.

 No.56

>>48

good


 No.59

hmm


 No.60

mm




File: 1446090298336.jpg (29.43 KB, 620x348, 155:87, 1400287271278942.jpg)

 No.47[Reply]

Scientists present new recipes for directly converting glial cells to neurons in mouse brains.

Adult human brains have a very limited ability to produce new neurons, so scientists have been pursuing ways to convert other types of brain cells into these coveted cell types. Several presentations at this week’s Society for Neuroscience (SfN) meeting held in Chicago demonstrated that it’s possible to reprogram glia—non-neuronal cells known for supporting their neuron neighbors—into neurons within the brains of mice.

Sophie Peron of Johannes Gutenberg University in Germany took the genes for two transcription factors, Sox 2 and Ascl1, and overexpressed them in the cortices of mice. She found that 15 percent of the mouse glia cells turned into neurons.

The features of these new neurons are still to be worked out, Peron said. “That’s the next step. Now that we have a system to get these cells converted we are currently studying their connectivity, functionality, and precise characteristics,” she told The Scientist.

Peron said any potential therapy using reprogrammed cells would have to be able to produce specific neural subtypes, which may require additional steps to guide the cells in the right direction.

Other groups are working to convert reactive astrocytes—a form of glial cells that come to the aid of neurons after an injury, such as stroke—into neurons. Although these cells protect neurons from dying, they can crowd the area to create a sort of scar that impedes a full recovery.

Chun-Li Zhang of the University of Texas Southwestern Medical Center described a method to convert reactive astrocytes to neurons via Sox 2. “Patch-clamp recordings from the induced neurons reveal subtype heterogeneity, though all are functionally mature, fire repetitive action potentials, and receive synaptic inputs,” Zhang wrote in his SfN abstract.

In another presentation, Penn State University’s Gong Chen and Yuchen Chen described administering a gene for the transcription factor NeuroD1 into the cortices of mice that had experienced strokes. Following the treatment, the researchers found that glial scar and atrophy in the cortex were reduced. “These findings suggest that direct reprogramming oPost too long. Click here to view the full text.

 No.51

Sweet


 No.52

>>47

External brain HDD when?


 No.53

>>52

is that safe?




 No.50[Reply]

Genetic Engineering & NanoBioTechnology

We are rapidly approaching an era when it may not only be possible but also insuppressible that people will be able to modify their genes at low cost.

In decades to come, however much the well meaning worry about the nefarious applications of gene editing, the needs of the sick will continue to drive science and medicine forward - as they should.

Researchers are beginning to understanding how the animals maintain their hundreds of teeth throughout their adult lives. By studying how structures in embryonic fish differentiate into either teeth or taste buds, the researchers hope to one day be able to turn on the tooth regeneration mechanism in humans - which, like other mammals, get only two sets of teeth to last a lifetime.

https://archive.is/LDjBy

Still, today, there are those who fear genetic engineering.

"Genetic alteration is never predictable and can result in oversized embryos, resulting in painful births. It can leave the animals severely affected in a way which is impractical for life. The process also very wasteful."

In reference to the dog study, Hawkins said, "The genetic alteration of animals simply to make them stronger, or to have greater running ability, is completely unacceptable.

https://archive.is/eySjI

Viruses are a more nuanced scalpel – they have an evolutionarily vetted mode of entry and expression. To avoid the unsavory bursting cell scenario, “replication-deficient” viruses have been engineered. Given these strategic advantages, and spurred on by the enhanced editing capabilities enabled by CRISPR-based nucleases, Xiaoyu Chen and Manuel Goncalves at Leiden University Medical Center recently published a review of viral vectors as gene editing tools in Molecular Therapy. They highlight three types of viruPost too long. Click here to view the full text.



File: 1446093162496.jpg (43.32 KB, 559x311, 559:311, 1438904568965.jpg)

 No.48[Reply]

Researchers have selectively activated a specific neural pathway to manipulate a primate’s behavior

WIKIMEDIA, J.M. GARGScientists have used optogenetics to target a specific neural pathway in the brain of a macaque monkey and alter the animal’s behavior. As the authors reported in Nature Communications last month, such a feat had been accomplished only in rodents before.

Optogenetics relies on the insertion of a gene for a light-sensitive ion channel. When present in neurons, the channel can turn on or off the activity of a neuron, depending on the flavor of the channel. Previous attempts to use optogenetics in nonhuman primates affected brain regions more generally, rather than particular neural circuits. In this case, Masayuki Matsumoto of Kyoto University and colleagues delivered the channel’s gene specifically to one area of the monkey’s brain called the frontal eye field.

They found that not only did the neurons in this region respond to light shone on the brain, but the monkey’s behavior changed as well. The stimulation caused saccades—quick eye movements. “Our findings clearly demonstrate the causal relationship between the signals transmitted through the FEF-SC [frontal eye field-superior colliculus] pathway and saccadic eye movements,” Matsumoto and his colleagues wrote in their report.

“Over the decades, electrical microstimulation and pharmacological manipulation techniques have been used as tools to modulate neuronal activity in various brain regions, permitting investigators to establish causal links between neuronal activity and behaviours,” they continued. “These methodologies, however, cannot selectively target the activity (that is, the transmitted signal) of a particular pathway connecting two regions. The advent of pathway-selective optogenetic approaches has enabled investigators to overcome this issue in rodents and now, as we have demonstrated, in nonhuman primates.”

https://archive.is/Dmow9



File: 1445463309602.jpg (5.81 KB, 276x183, 92:61, rock.jpg)

 No.43[Reply]

Do rocks have genes?

You can divide them to infinity and it's still a rock

Something makes them keep their form somehow



File: 1445456354345.jpg (128.16 KB, 500x886, 250:443, tri glide.jpg)

 No.42[Reply]

Genomic loop formation is a well-documented method that the cellular machinery uses to regulate the expression of various genes within human chromosomes. Yet, how these loops form and fold has eluded scientists for a number of years.

Now, researchers based at Houston's Texas Medical Center have found that a protein complex that forms the gene regulatory loop works like the sliding plastic adjusters on a grade schooler's backpack—a discovery that could provide new clues about genetic diseases and allow researchers to reprogram cells by directly modifying the loops in genomes.

"For months, we had no idea what our data really meant," explained senior author Erez Lieberman-Aiden, Ph.D., geneticist and computer scientist with joint appointments at Baylor and Rice Universities. "Then one day, we realized that we'd been carrying the solution around—literally, on our back—for decades!"

The findings from this study were published online recently in PNAS through an article entitled “Chromatin extrusion explains key features of loop and domain formation in wild-type and engineered genomes.”

Since many genes are activated by loops, it is impossible to understand gene activation without knowing how loops form. With that in mind, the researchers found a set of proteins that acts like the plastic slider, sometimes called a tri-glide, which adjusts a backpack strap.

"The protein complex that forms DNA loops appears to operate like the plastic slider that is used to adjust the length of the straps: it lands on DNA and takes up the slack to form a loop," noted co-first author Adrian Sanborn, graduate student in Dr. Aiden’s laboratory.

Because of their computer science and computational mathematics background, the investigators were able to create a tri-glide model to predict how a genome would fold. The team confirmed their predictions by making tiny modifications in a cell's genome and showing that the mutations changed the folding pattern exactly as expected.

"We found that changing even one letter in the genetic code was enough to modify the folding of millions of other letters," said co-first author Suhas Rao, graduate student in Dr. Aiden’s laboratory. "What was stunning was thatPost too long. Click here to view the full text.



File: 1445442497561.jpg (104.07 KB, 1200x358, 600:179, CrypticVariants.jpg)

 No.41[Reply]

Disruption of certain genes can reveal cryptic genetic variants that do not typically show phenotypic effects. Because this phenomenon, which is referred to as ‘phenotypic capacitance’, is a potential source of trait variation and disease risk, it is important to understand how it arises at the genetic and molecular levels. Here, we use a cryptic colony morphology trait that segregates in a yeast cross to explore the mechanisms underlying phenotypic capacitance. We find that the colony trait is expressed when a mutation in IRA2, a negative regulator of the Ras pathway, co-occurs with specific combinations of cryptic variants in six genes. Four of these genes encode transcription factors that act downstream of the Ras pathway, indicating that the phenotype involves genetically complex changes in the transcriptional regulation of Ras targets. We provide evidence that the IRA2 mutation reveals the phenotypic effects of the cryptic variants by disrupting the transcriptional silencing of one or more genes that contribute to the trait. Supporting this role for the IRA2 mutation, deletion of SFL1, a repressor that acts downstream of the Ras pathway, also reveals the phenotype, largely due to the same cryptic variants that were detected in the IRA2 mutant cross. Our results illustrate how higher-order genetic interactions among mutations and cryptic variants can result in phenotypic capacitance in specific genetic backgrounds, and suggests these interactions might reflect genetically complex changes in gene expression that are usually suppressed by negative regulation.

Some genetic polymorphisms have phenotypic effects that are masked under most conditions, but can be revealed by mutations or environmental change. The genetic and molecular mechanisms that suppress and uncover these cryptic genetic variants are important to understand. Here, we show that a single mutation in a yeast cross causes a major phenotypic change through its genetic interactions with two specific combinations of cryptic variants in six genes. This result suggests that in some cases cryptic variants themselves play roles in revealing their own phenotypic effects through their genetic interactions with each other and the mutations that reveal them. We also demonstrate that most of the genes harboring cryptic variation in our system are transcription factors, a finding that supports an important role for pPost too long. Click here to view the full text.



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