Tag Archives: genetics

THE DNA OF GOD?

This article interested me for the ideas presented. For I have long believed that human DNA is simply an expression of Divine DNA in an imperfect form that could be rearranged and made as God originally intended, through both the agency of Christ and through human effort (for it also requires the effort and desire of the individual so involved).

I am still unresolved on the issue of whether this Divine DNA pattern already exists within us and must simply be recombined into a pattern and form that matches that of Christ, or if Christ’s DNA (pattern), for lack of a better term, must replace ours because ours has become so corrupted or mutated that at least some bad strands must be excised and thereafter entirely replaced (a sort of genetic “transplant” – again for lack of a better term).

A divine fusion takes place when Holy Spirit meets your human spirit.
A divine fusion takes place when Holy Spirit meets your human spirit. (Flickr )

Understanding the new creation reality is so vital to an overcoming Christian life. If you don’t know who you really are, you can never experience the fullness of abundant life in Christ.

We’ve heard it preached our entire Christian lives, “You are a new creation! Old things have passed away and all things have become new!” But do we really understand what this means? When we come to Christ, does God just make us better versions of ourselves? Or does something much more profound happen?

A Divine Fusion Takes Place

Recently God gave me a vision of what happens to us at salvation and it radically altered the way I see myself. I saw the moment God encountered Mary in Luke 1:31-35 telling her she would bear the Christ Child. I saw the person of the Holy Spirit overshadow her. I saw Mary’s DNA and the Holy Spirit’s DNA. I saw them intertwine and become one, creating Jesus in her womb, fully God and fully man.

Then the vision shifted to me. I saw myself at salvation. I saw the Holy Spirit overshadow me and fill me. My body became the temple of the Holy Spirit. I also saw my spirit man’s DNA and the Holy Spirit’s DNA. I saw them intertwine and become one.

I saw the Holy Spirit wrap around my human spirit like two DNA strands coming together as one, just like when the DNA from a father and mother mix together to form a new baby. It looked like the Double Helix. As the Holy Spirit wrapped around my human spirit, they fused together, becoming one and forming a brand new creation. This fusion of Holy Spirit and my human spirit formed Christ in me!

Heavenly DNA—Divine Nature

1 Corinthians 6:17 declares, “But he who is joined to the Lord becomes one spirit with Him” (MEV). This revelation was in Scripture the whole time! I became one spirit with the Holy Spirit and I now have a new holy, divine nature.

This is Christ in me, the hope of glory (Col 1:27, 2 Pet 1:4). Divine DNA from God was fused into my human spirit causing me to become a partaker of God’s divine nature! I was truly a brand new creation. As Holy Spirit became one with my human spirit, I was “born again” and Christ was formed inside of me. I was much more than a better version of myself. I was something brand new!

When you receive Christ as your Savior and the Holy Spirit takes up residence inside of you, He actually fuses Himself together with your spirit. You become one with God! You have His divine nature inside of you. You are a brand new creation, with new desires and a new life. Your core identity is completely transformed. Christ’s very nature and identity is now completely formed in your spirit. It’s a glorious transformation! This is why you are holy, righteous and clean!

I have so much more to teach you on this amazing subject. I have just put together a teaching series called Divine DNA—New Creation Reality. I think it’s one of the most important teachings I have ever done. Having divine DNA in your spirit has so many effects on your life as you become transformed in your spirit, soul and body.

I encourage you with all my heart to sow this teaching into your mind and heart today and learn who you really are! Once you know who you are, the devil will never be able to lie to you again and you will walk in power, victory and freedom.

GIVING MEN AND WOMEN “THE FINGER”

What the Length of Your Ring Finger Can Tell You About Your Masculinity

hand_header

Stop what you’re doing and look at your hands.

Is your ring finger longer than your index finger?

If so, you were likely exposed to higher levels of testosterone while you were in your mother’s womb.

Is your index finger longer than your ring finger?

Then you were exposed to lower levels of T as a fetus.

So what?

Well, while it might sound like hokey palm reading, researchers are finding that the ratio between the length of your ring and index fingers may in fact correlate to your prenatal exposure to T, and have a significant influence on your body, brain, and behavior well into adulthood.

How strong is this correlation and what exactly does it foretell? I’ve dived deep into all the available research to sort myth from fact, and present this comprehensive look at what digit ratio really means for your masculinity.

Prenatal Testosterone, Androgen Receptors, and 2D:4D Finger Ratios

2D/4D finger digit ratios diagram index finger and ring finger

Scientists have long noticed that men’s ring fingers are generally longer than their index fingers. With women, it tends to be the reverse: their index fingers are usually longer. They’ve called this difference in length between the index finger and ring finger the “2D:4D ratio.”

2D stands for “second digit” — that’s your index finger, and 4D means “fourth digit” — your ring finger. So if your index finger is 2.9 inches long and your ring finger is 3.1 inches long, you have a 2D:4D ratio of .935 (2.9/3.1 = .935). A longer ring finger compared to your index finger is considered a “low 2D:4D ratio.”

If your index finger is 3.1 inches long and your ring finger is 2.9 inches long, your 2D:4D ratio would be 1.06 (3.1/2.9 = 1.06). A longer index finger compared to your ring finger is considered a “high 2D:4D ratio.”

Digit ratios lie on a spectrum. Some men have really low digit ratios, like .83, and some folks have really high digit ratios, like 1.06.

The Connection Between 2D:4D Ratio and Prenatal Hormones

While scientists during the mid-20th century were able to statistically establish this general difference between men’s and women’s 2D:4D ratios, it wasn’t until the 1980s that researchers began speculating as to why this sex difference exists and how 2D:4D ratios may correlate with different gender traits. Dr. Glenn Wilson of King’s College was one of the first to hypothesize that 2D:4D finger ratio was determined by sex hormone exposure in the womb.

In 1998, further strides were made when psychologist John Manning of the University of Liverpool (now at Swansea University) published a paper in which he hypothesized that 2D:4D ratios are determined by prenatal exposure to testosterone. Other researchers came to similar conclusions using corollary evidence.

It wasn’t until 2011, however, that scientists were able to directly show that prenatal exposure to testosterone determines the 2D:4D ratio. While prenatal testing and studies are difficult-to-impossible to ethically conduct on human fetuses, the general difference between 2D:4D ratios in human males and females also exists between the sexes of other animals. Consequently, animal studies can provide insight into why these general differences exist.

Developmental biologists Martin Cohn and Zhengui Zheng conducted experiments on fetal mice in which they modified the amounts of testosterone they were exposed to in utero. What they discovered is that it’s not just the amount of fetal testosterone that determines digit ratio, but rather the balance between testosterone and estrogen. Mice with higher testosterone concentrations or low estrogen levels had more male-like digit ratios (low 2D:4D ratio), while mice with higher estrogen levels or low testosterone levels had higher, more feminine digit ratios (high 2D:4D ratios).

manning-2D-4D-digit-ratio-theory

Cohn and Zheng posit that what’s true for mice is true for humans as well: prenatal exposure to a mixture of testosterone and estrogen is what determines 2D:4D ratios. So the lower your 2D:4D digit ratio is, the more testosterone or less estrogen you were exposed to in the womb. The higher your 2D:4D ratio, the less testosterone or more estrogen you were exposed to as a fetus.

What Causes Differences in the Levels of Sex Hormones in the Womb?

What causes these differences in the levels of sex hormones in the womb? Scientists aren’t yet sure, though they have some hunches. Genetics certainly play a role, both of the mother and the fetus. For one thing, some research suggests that mothers with elevated testosterone levels influence the testosterone levels of their daughters (but there appears to be no such influence with maternal testosterone on boys). Some research has also found that the first-born child, whether male or female, is exposed to more estrogen prenatally, for reasons we don’t yet understand.

Environmental factors are in play as well. For example, fetal testosterone levels are elevated in both males and females if the mother smokes during pregnancy, but are lower if the mother consumes alcohol. A mother may also expose her baby to more estrogen in the womb if she herself is exposed to a high level of “xenoestrogens,” chemicals that imitate estrogens in the body, and that are found in nearly everything – from plastics and gasoline to cosmetics and shampoo.

The timing and duration of a fetus’ exposure to sex hormones matter, too. If testosterone surges a little too late or early, the result can be a male fetus that is male in both body and mind but isn’t as masculinized as he would be if the T surge had happened at the usual time.

Duration of exposure may also influence how masculine or feminine your 2D:4D ratio is and consequently, how masculine and feminine your body and mind end up. Different parts of the fetal body and brain are open to androgen sensitivity at different times during gestation. It’s possible that you had a high testosterone to estrogen exposure during the period in which penis formation occurs, but for some reason, it started to peter out when 2D:4D formation happens or when other sex parts of the body and mind are receptive to androgen. Consequently, you end up with a higher, more female-like 2D:4D ratio despite being very masculine in other areas.

What affects the timing and duration of the release of sex hormones in utero? Here again, researchers really aren’t sure.

While scientists don’t definitively know why some individuals are exposed to greater and lesser amounts of estrogen and testosterone in the womb, they do know that 2D:4D ratios are directly caused by the make-up of this hormonal mixture, and can use these ratios to explore possible correlations between prenatal sex hormone exposure and other psychological and physiological traits in individuals later on in life. Testosterone, in particular, has what scientists call an “organizational effect” on the human mind and body — exposure to it during sensitive periods in utero has permanent effects on mind, body, and behavior. Let’s take a closer look at what some of those effects might be.

Correlations Between Gender Traits and 2D:4D Ratio

Below, I highlight some of the possible correlations between your digit ratio and traits that we often define as “masculine” and “feminine.”

But first, a caveat. While researchers have found correlations between 2D:4D ratios and specific sex characteristics, they also note that these correlations are sometimes weak. What’s more, some relationships between 2D:4D ratios and sex traits that have been found in the past, haven’t been replicated in other studies.

What’s more, it can’t be emphasized enough that these are correlational studies, and as we all know, correlation does not equal causation. In many of the popular media articles I’ve read about this subject and its influence on different traits, digit ratio is often presented as deterministic. I can see lots of people reading these articles and looking at their fingers and thinking, “Well, my index finger is longer than my ring finger. I’m destined to be a girly man for the rest of my life.”

But gender isn’t as simple as that. Yes, biology plays a role and prenatal sex hormone exposure appears to have an influence on the masculinization or feminization of an individual throughout his or her life. But the biological component of gender is complex. As discussed above, it’s not just the ratio of testosterone and estrogen you were exposed to prenatally that may influence gender traits, but also the timing and duration of that exposure which plays a role too. Also, the T surge at puberty has a dramatic effect on masculinizing the body. What’s more, we can’t discount the environmental influences on gender that we all experience in our life, from our culture to our home environment to the choices we make.

So, as you look through the insights below, avoid the temptation to read too much into them. Take them as food for thought and something to consider — one tool among many in getting to know yourself better.

Note: As you read this, keep in mind that 2D:4D ratio is used as a corollary to testosterone/estrogen exposure in the womb. When you read “low 2D:4D,” think “higher testosterone/lower estrogen prenatal exposure,” and when you read “high 2D:4D,” think “lower testosterone/higher estrogen prenatal exposure.”

Aggression

Several correlational studies have found that individuals with a lower 2D:4D ratio tend to be more aggressive than people with higher 2D:4D ratios. The theory is that exposure to prenatal testosterone has organizational effects on the brain that “masculinize” it and make it more prone to aggressive behavior.

How Well Men Get Along With Women

Recent research has found that men with lower 2D:4D ratios are nicer to women than men with higher 2D:4D ratios. According to the study’s lead author, Debbie Moskowitz, “when with women, men with smaller ratios were more likely to listen attentively, smile and laugh, compromise, or compliment the other person.” Men with higher 2D:4D ratios tend to have a more difficult time getting along with women.

A follow-up study by another group of researchers found that men with lower 2D:4D ratios make greater efforts to impress women while courting them compared to men with higher 2D:4D ratios. They’re more likely to buy things like flowers and spend more on dates. What’s more, men with low 2D:4D ratios tend to spend more time and money on their appearance than men with higher 2D:4D ratios.

These findings might seem counterintuitive: wouldn’t a more masculine, “alpha” man have trouble getting along with women, and not care about things like style and romance? And wouldn’t a more feminized man find it easier to get along with women?

A man with more T, however, may be more driven to reproduce, and is thus more motivated to learn how to woo women, while men with lower T have less of this drive, and thus care less about their success with the ladies.

It’s interesting to note that researchers also found that women with higher, more feminized 2D:4D ratios were more likely to put greater effort into attracting men by staying fit, and wearing make-up and stylish clothes. Women with lower 2D:4D ratios (who tend to grow up as tomboys) don’t put in as much effort.

These correlational studies between digit ratio and mating effort may explain why men with lower 2D:4D digit ratios tend to marry younger and have more children than men with higher 2D:4D ratios — they’re more likely to do the courting necessary to find a mate.

The Type of Woman You Marry (Depending on Environment)

In one study among the semi-nomadic Himba population in Northern Namibia, researchers found that both men and women with lower, more masculine 2D:4D ratios tended to marry younger than men and women with higher, more feminized 2D:4D ratios.

The fact that Himba women with more masculine digit ratios were more likely to be married than women with more feminized digit ratios is another finding that may seem counterintuitive. You’d think the men would be more attracted to the more feminine women. The researchers suggest that men who live in harsh, resource-poor environments choose more masculine women, selecting for the traits that will aid their partnership in survival. In peaceful, resource-abundant times, men have the luxury of choosing mates who are not as hardy, but are more attractive and feminine (and often have a high 2D:4D ratio).

Fidelity

Several studies suggest that both men and women with lower 2D:4D ratios tend to be more promiscuous than men and women with higher 2D:4D ratios, suggesting prenatal exposure to testosterone can influence sexual behavior into adulthood.

Athletic Ability

Dr. Manning has published several research articles showing correlations between low 2D:4D ratio and improved athletic ability across sports. In fact, the lower the 2D:4D ratio gets, the more athletic ability tends to improve.

For example, Dr. Manning found that low 2D:4D digit ratio correlates with running speed. He actually put his reputation as the “finger scientist” on the line on the BBC, when he predicted who would win a sprinting race simply by looking at photographic copies of the competitors’ hands. He got 4 out of 6 right; the two he got wrong finished close together.

Sports that involve balls require an ability to make quick visual-spatial judgments as to where a ball is going to land; Manning has found that men with lower 2D:4D ratios perform better on tests of visual-spatial ability. He theorizes that prenatal exposure to testosterone influences the central nervous system to improve the capacity to make these visual-spatial decisions.

Manning has also found that star players in professional soccer teams in the United Kingdom typically have lower 2D:4D ratios than the teams’ reserve players.

Risk Taking

Several studies have found that a lower 2D:4D ratio is correlated with risk taking in men. For example, one study found that men with lower 2D:4D ratios were more likely to engage in “social and recreational” risks than men with higher 2D:4D ratios. Social risks are things like “speaking your mind about an unpopular issue at a social occasion” and recreational risks are things like taking part in mountain climbing or skydiving. The research found the correlation in men only. No such relationship existed in women, even those with lower 2D:4D ratios.

Another study found that men with lower 2D:4D ratios performed better in high-frequency stock trading, partly because they were more likely to take financial risks than men with higher 2D:4D ratios. I’d be curious to see a similar study on differences in financial performance between individuals with low and high 2D:4D ratios on long-term investing. I suspect that people with higher 2D:4D ratios would do better.

Smoking and Drinking

Since the 19th century, smoking has often been associated with manliness, but in onestudy, Manning found that individuals with higher, more feminized 2D:4D ratios actually smoked more than people with lower, more masculine 2D:4D ratios.

With alcohol consumption, low 2D:4D ratios correlate with higher drinking and alcohol dependence, while high 2D:4D ratios correlate with lower drinking and alcohol dependence.

Musical Ability

When studying the male members of an orchestra, Manning found that a lower 2D:4D ratio correlated with chair position; that is, the men with lower 2D:4D ratios tended to be ranked near the top in the orchestra. No such correlation between low 2D:4D ratio and musical ability existed with women. In fact, a similar study performed by another group of researchers which focused on female orchestral musicians found that female musicians with higher, more feminized 2D:4D ratios ranked higher in the orchestra.

Autism

Autism researcher Simon Baron-Cohen has called autism a manifestation of the “extreme male brain.” Males are diagnosed with autism at a much higher frequency than females, and many of the traits that individuals on the autism spectrum manifest are typical male traits, amplified. For example, individuals on the autism spectrum tend to show strengths in mathematical and spatial reasoning. They also tend to have a higher risk of language impairment and a hard time in social situations.

Manning and Baron-Cohen teamed up on a study to see if there’s a correlation between 2D:4D ratio and autism, and indeed they found one: children with autism had a lower 2D:4D ratio compared to population normative digit ratios. While the causes of autism spectrum are complex, and there’s likely no single cause, this study suggests that prenatal exposure to testosterone may play a role.

Verbal Fluency

Individuals with higher, feminized 2D:4D ratios have more verbal fluency than people with lower 2D:4D ratio.

ADHD

If you have a hard time focusing and sitting still, your exposure to prenatal sex hormones may be partly to blame. Studies have found correlations between low 2D:4D ratios and ADHD.

Risk of Depression and Anxiety

Elevated testosterone levels have been shown to blunt depression and anxiety in adult men and women. 2D:4D research suggests that prenatal testosterone exposure may organize the brain in such a way as to make an individual more or less susceptible to depression and anxiety as adults. Studies have found that men and women with higher, more feminized 2D:4D ratios have a higher risk of developing depression and anxiety compared to individuals with lower, more masculine 2D:4D ratios.

Risk for Heart Disease

As we discussed in our post about the benefits of testosterone, optimal levels of T as a grown man reduces the risk of developing heart disease. But research suggests that testosterone’s heart-protecting benefits may begin while you’re still a fetus. One study found that men with lower 2D:4D ratios have a reduced risk of developing heart disease compared to men with higher ratios.

Risk for Obesity

Elevated testosterone levels can ward off obesity as an adult, but elevated T levels in the womb may program the body to fight fat later in life as well. Research has found that men with lower 2D:4D ratios tend to be less obese than men with higher 2D:4D levels.

Masculinized or Feminized Face

Masculine faces, according to researchers, are more “robust.” The jaw is wider, the forehead is smaller and shorter, the nose is broader and thicker, eyebrows are thicker, and the eyes are closer together. Basically, your head looks like Thwomp from Super Mario. OrJocko Willink.

Feminine faces are characterized by large foreheads, long slim eyebrows, narrow cheeks, pointier jaws, and eyes that are further apart. On males, these features make them look more pixie, or Peter Pan-like.

Researchers believe that the testosterone surge which occurs at puberty is what gives men their masculine-looking faces. And it does. When boys hit puberty, their little chubby, round mugs start looking more like Thwomp. But one study suggests that prenatal testosterone exposure sets the stage for how masculine a male’s face will be at puberty. In fact, differences in how masculine a boy’s face is can be seen even before puberty, and as you might have guessed, 2D:4D ratio correlates with it.

When researchers looked at a group of boys ages 4-11 and measured their faces for masculine or feminine features, they found that boys with a more masculine, square-shaped head had a lower 2D:4D ratio, while boys with a slenderer, feminine face had a higher 2D:4D ratio.

Testosterone Levels as Adults

We’ve written extensively about the benefits of optimal testosterone levels and the lifestyle changes you can make to ensure that your levels are at their peak. But does prenatal testosterone exposure influence testosterone levels as a grown man?

Most studies have found no correlation between 2D:4D ratio and adult testosterone levels. So whether you have a masculine, low 2D:4D ratio or a more feminine, high 2D:4D ratio won’t affect the amount of circulating testosterone in your body as a grown man.

Manning conducted one study that suggests higher 2D:4D ratios may be correlated with less androgen sensitivity. According to this conclusion, if you were exposed to less prenatal testosterone as a fetus, your body simply won’t respond as much to testosterone compared to men with lower, more masculine 2D:4D ratios.

However, a follow-up study by another researcher found no such correlation.

So bottom line: if you’ve got a higher 2D:4D ratio, don’t worry about it lowering your total and free testosterone levels as a grown man.

Penis Length

A recent study out of South Korea found a correlation between 2D:4D ratio and penis length. Men with lower 2D:4D ratios tend to have longer penises when flaccid, while men with higher 2D:4D ratios have shorter penises. The researchers called for more studies on penis length and 2D:4D ratio in men from other countries.

Risk for Prostate Cancer

It may seem like most of the benefits cut the way of those with a lower 2D:4D ratio, but here’s one that goes the other way. We know that elevated testosterone levels in adult men increase the risk of prostate cancer. But research suggests that exposure to T while in the womb may also influence your chances of getting prostate cancer as an adult. A few studieshave shown that men with lower 2D:4D ratios have a higher risk of prostate cancer and other prostate diseases than men with higher 2D:4D ratios.

Sexual Orientation

One of the most common correlations the popular media likes to talk about in regards to 2D:4D ratios is the link to sexual orientation. But is there really a connection? Research shows mixed conclusions — especially with men.

Among males, some studies have found that men with higher 2D:4D ratios are more likely to identify as gay. But other studies found that homosexual men tend to have lower 2D:4D ratios than heterosexual men. Still other research found that the correlation between 2D:4D ratio and sexual orientation depends on the country a man lives in. Finally, a meta-analysisof all these different studies about sexual orientation and 2D:4D ratio found no significant correlations.

Basically, you can’t look at a man’s hands and determine if he’s gay or straight.

With women, however, several studies have found that lesbians, particularly those who identify as “butch,” have lower 2D:4D ratios than heterosexual women or more feminine lesbians.

At the end, I want to reiterate that while all this information and these hypotheses are interesting, they’re correlational and not strictly deterministic. If you have a high 2D:4D ratio, it shouldn’t be reason for insecurity. The duration of hormones you received in the womb may have made you masculine in other ways, but missed your fingers. And even if you ultimately didn’t bathe in as much T as a fetus, that doesn’t mean you can’t be manly as an adult. Masculinity, after all, comes together at the crossroads between biology and choice. Follow Pindar’s advice. Accept what nature has given you, and “become who you are.”

THE CODE WITHIN – BODY OF EVDIENCE

I’ve long suspected something like this… and I don’t see at all how it could be a surprise, after all it is readily available raw material, just not always actualized or properly arranged material.

It is a lot easier than seeking out and incorporating alien or foreign genetic material.

 

A Surprise Source of Life’s Code

Emerging data suggests the seemingly impossible — that mysterious new genes arise from “junk” DNA.

[No Caption]

Genes, like people, have families — lineages that stretch back through time, all the way to a founding member. That ancestor multiplied and spread, morphing a bit with each new iteration.

For most of the last 40 years, scientists thought that this was the primary way new genes were born — they simply arose from copies of existing genes. The old version went on doing its job, and the new copy became free to evolve novel functions.

Certain genes, however, seem to defy that origin story. They have no known relatives, and they bear no resemblance to any other gene. They’re the molecular equivalent of a mysterious beast discovered in the depths of a remote rainforest, a biological enigma seemingly unrelated to anything else on earth.

The mystery of where these orphan genes came from has puzzled scientists for decades. But in the past few years, a once-heretical explanation has quickly gained momentum — that many of these orphans arose out of so-called junk DNA, or non-coding DNA, the mysterious stretches of DNA between genes. “Genetic function somehow springs into existence,” said David Begun, a biologist at the University of California, Davis.

New genes appear to burst into existence at various points along the evolutionary history of the mouse lineage (red line). The surge around 800 million years ago corresponds to the time when earth emerged from its “snowball” phase, when the planet was almost completely frozen. The very recent peak represents newly born genes, many of which will subsequently be lost. If all genes arose via duplication, they all would have been generated soon after the origins of life, roughly 3.8 billion years ago (green line).

This metamorphosis was once considered to be impossible, but a growing number of examples in organisms ranging from yeast and flies to mice and humans has convinced most of the field that these de novo genes exist. Some scientists say they may even be common. Just last month, research presented at the Society for Molecular Biology and Evolution in Vienna identified 600 potentially new human genes. “The existence of de novo genes was supposed to be a rare thing,” said Mar Albà, an evolutionary biologist at the Hospital del Mar Research Institute in Barcelona, who presented the research. “But people have started seeing it more and more.”

Researchers are beginning to understand that de novo genes seem to make up a significant part of the genome, yet scientists have little idea of how many there are or what they do. What’s more, mutations in these genes can trigger catastrophic failures. “It seems like these novel genes are often the most important ones,” said Erich Bornberg-Bauer, a bioinformatician at the University of Münster in Germany.

The Orphan Chase

The standard gene duplication model explains many of the thousands of known gene families, but it has limitations. It implies that most gene innovation would have occurred very early in life’s history. According to this model, the earliest biological molecules 3.5 billion years ago would have created a set of genetic building blocks. Each new iteration of life would then be limited to tweaking those building blocks.

Yet if life’s toolkit is so limited, how could evolution generate the vast menagerie we see on Earth today? “If new parts only come from old parts, we would not be able to explain fundamental changes in development,” Bornberg-Bauer said.

The first evidence that a strict duplication model might not suffice came in the 1990s, when DNA sequencing technologies took hold. Researchers analyzing the yeast genome found that a third of the organism’s genes had no similarity to known genes in other organisms. At the time, many scientists assumed that these orphans belonged to families that just hadn’t been discovered yet. But that assumption hasn’t proven true. Over the last decade, scientists sequenced DNA from thousands of diverse organisms, yet many orphan genes still defy classification. Their origins remain a mystery.

In 2006, Begun found some of the first evidence that genes could indeed pop into existence from noncoding DNA. He compared gene sequences from the standard laboratory fruit fly, Drosophila melanogaster, with other closely related fruit fly species. The different flies share the vast majority of their genomes. But Begun and collaborators found several genes that were present in only one or two species and not others, suggesting that these genes weren’t the progeny of existing ancestors. Begun proposed instead that random sequences of junk DNA in the fruit fly genome could mutate into functioning genes.

Diethard Tautz, a biologist at the Max Planck Institute for Evolutionary Biology, once doubted whether de novo genes could exist. He now thinks they may actually be quite common.

Yet creating a gene from a random DNA sequence appears as likely as dumping a jar of Scrabble tiles onto the floor and expecting the letters to spell out a coherent sentence. The junk DNA must accumulate mutations that allow it to be read by the cell or converted into RNA, as well as regulatory components that signify when and where the gene should be active. And like a sentence, the gene must have a beginning and an end — short codes that signal its start and end.

In addition, the RNA or protein produced by the gene must be useful. Newly born genes could prove toxic, producing harmful proteins like those that clump together in the brains of Alzheimer’s patients. “Proteins have a strong tendency to misfold and cause havoc,” said Joanna Masel, a biologist at the University of Arizona in Tucson. “It’s hard to see how to get a new protein out of random sequence when you expect random sequences to cause so much trouble.” Masel is studying ways that evolution might work around this problem.

Another challenge for Begun’s hypothesis was that it’s very difficult to distinguish a true de novo gene from one that has changed drastically from its ancestors. (The difficulty of identifying true de novo genes remains a source of contention in the field.)

Ten years ago, Diethard Tautz, a biologist at the Max Planck Institute for Evolutionary Biology, was one of many researchers who were skeptical of Begun’s idea. Tautz had found alternative explanations for orphan genes. Some mystery genes had evolved very quickly, rendering their ancestry unrecognizable. Other genes were created by reshuffling fragments of existing genes.

Then his team came across the Pldi gene, which they named after the German soccer player Lukas Podolski. The sequence is present in mice, rats and humans. In the latter two species, it remains silent, which means it’s not converted into RNA or protein. The DNA is active or transcribed into RNA only in mice, where it appears to be important — mice without it have slower sperm and smaller testicles.

The researchers were able to trace the series of mutations that converted the silent piece of noncoding DNA into an active gene. That work showed that the new gene is truly de novo and ruled out the alternative — that it belonged to an existing gene family and simply evolved beyond recognition. “That’s when I thought, OK, it must be possible,” Tautz said.

A Wave of New Genes

Scientists have now catalogued a number of clear examples of de novo genes: A gene in yeast that determines whether it will reproduce sexually or asexually, a gene in flies and other two-winged insects that became essential for flight, and some genes found only in humans whose function remains tantalizingly unclear.

The Odds of Becoming a Gene

Scientists are testing computational approaches to determine how often random DNA sequences can be mutated into functional genes. Victor Luria, a researcher at Harvard, created a model using common estimates of the rates of mutation, recombination (another way of mixing up DNA) and natural selection. After subjecting a stretch of DNA as long as the human genome to mutation and recombination for 100 million generations, some random stretches of DNA evolved into active genes. If he were to add in natural selection, a genome of that size could generate hundreds or even thousands of new genes.

At the Society for Molecular Biology and Evolution conference last month, Albà and collaborators identified hundreds of putative de novo genes in humans and chimps — ten-fold more than previous studies — using powerful new techniques for analyzing RNA. Of the 600 human-specific genes that Albà’s team found, 80 percent are entirely new, having never been identified before.

Unfortunately, deciphering the function of de novo genes is far more difficult than identifying them. But at least some of them aren’t doing the genetic equivalent of twiddling their thumbs. Evidence suggests that a portion of de novo genes quickly become essential. About 20 percent of new genes in fruit flies appear to be required for survival. And many others show signs of natural selection, evidence that they are doing something useful for the organism.

In humans, at least one de novo gene is active in the brain, leading some scientists to speculate such genes may have helped drive the brain’s evolution. Others are linked to cancer when mutated, suggesting they have an important function in the cell. “The fact that being misregulated can have such devastating consequences implies that the normal function is important or powerful,” said Aoife McLysaght, a geneticist at Trinity College in Dublin who identified the first human de novo genes.

Promiscuous Proteins

De novo genes are also part of a larger shift, a change in our conception of what proteins look like and how they work. De novo genes are often short, and they produce small proteins. Rather than folding into a precise structure — the conventional notion of how a protein behaves — de novo proteins have a more disordered architecture. That makes them a bit floppy, allowing the protein to bind to a broader array of molecules. In biochemistry parlance, these young proteins are promiscuous.

Scientists don’t yet know a lot about how these shorter proteins behave, largely because standard screening technologies tend to ignore them. Most methods for detecting genes and their corresponding proteins pick out long sequences with some similarity to existing genes. “It’s easy to miss these,” Begun said.

That’s starting to change. As scientists recognize the importance of shorter proteins, they are implementing new gene discovery technologies. As a result, the number of de novo genes might explode. “We don’t know what things shorter genes do,” Masel said. “We have a lot to learn about their role in biology.”

Scientists also want to understand how de novo genes get incorporated into the complex network of reactions that drive the cell, a particularly puzzling problem. It’s as if a bicycle spontaneously grew a new part and rapidly incorporated it into its machinery, even though the bike was working fine without it. “The question is fascinating but completely unknown,” Begun said. 

A human-specific gene called ESRG illustrates this mystery particularly well. Some of the sequence is found in monkeys and other primates. But it is only active in humans, where it is essential for maintaining the earliest embryonic stem cells. And yet monkeys and chimps are perfectly good at making embryonic stem cells without it. “It’s a human-specific gene performing a function that must predate the gene, because other organisms have these stem cells as well,” McLysaght said.

“How does novel gene become functional? How does it get incorporated into actual cellular processes?” McLysaght said. “To me, that’s the most important question at the moment.”

ADAPTIVE CRISPR

Comments? Good, or bad?

Or both?

Bioengineers develop tool for reprogramming genetic code

3 hours ago by Bjorn Carey
Bioengineers develop tool for reprogramming genetic code
Stanford bioengineers have developed a new tool that allows them to preferentially activate or deactivate genes in living cells. Credit: vitstudio/Shutterstock
Biology relies upon the precise activation of specific genes to work properly. If that sequence gets out of whack, or one gene turns on only partially, the outcome can often lead to a disease.

Now, bioengineers at Stanford and other universities have developed a sort of programmable genetic code that allows them to preferentially activate or deactivate genes in living cells. The work is published in the current issue of Cell, and could help usher in a new generation of gene therapies.

The technique is an adaptation of CRISPR, itself a relatively new genetic tool that makes use of a natural defense mechanism that bacteria evolved over millions of years to slice up infectious virus DNA.

Standard CRISPR consists of two components: a short RNA that matches a particular spot in the genome, and a protein called Cas9 that snips the DNA in that location. For the purposes of gene editing, scientists can control where the protein snips the genome, insert a new gene into the cut and patch it back together.

Inserting new , however, is just one way to influence how the genome is expressed. Another involves telling the cell how much or how little to activate a particular gene, thus controlling how much protein a cell produces from that gene and altering its behavior.

It’s this action that Lei Stanley Qi, an assistant professor of bioengineering and of chemical and systems biology at Stanford, and his colleagues aim to manipulate.

Influencing the genome

In the new work, the researchers describe how they have designed the CRISPR molecule to include a second piece of information on the RNA, instructing the molecule to either increase (upregulate) or decrease (downregulate) a target gene’s activity, or turn it on/off entirely.

Additionally, they designed it so that it could affect two different genes at once. In a cell, the order or degree in which are activated can produce different metabolic products.

“It’s like driving a car. You control the wheel to control direction, and the engine to control the speed, and how you balance the two determines how the car moves,” Qi said. “We can do the same thing in the cell by up- or downregulating genes, and produce different outcomes.”

As a proof of principle, the scientists used the technique to take control of a yeast metabolic pathway, turning genes on and off in various orders to produce four different end products. They then tested it on two mammalian genes that are important in cell mobility, and were able to control the cell’s direction and how fast it moved.

 

Future therapies

The ability to control genes is an attractive approach in designing genetic therapies for complex diseases that involve multiple genes, Qi said, and the new system may overcome several of the challenges of existing experimental therapies.

“Our technique allows us to directly control multiple specific and pathways in the genome without expressing new transgenes or uncontrolled behaviors, such as producing too much of a protein, or doing so in the wrong cells,” Qi said. “We could eventually synthesize tens of thousands of RNA molecules to control the genome over a whole organism.”

Next, Qi plans to test the technique in mice and refine the delivery method. Currently the scientists use a virus to insert the molecule into a cell, but he would eventually like to simply inject the molecules into an organism’s blood.

“That is what is so exciting about working at Stanford, because the School of Medicine’s immunology group is just around the corner, and working with them will help us address how to do this without triggering an immune response,” said Qi, who is a member of the interdisciplinary Stanford ChEM-H institute. “I’m optimistic because everything about this system comes naturally from , and should be compatible with any organism.”

Explore further: ‘CRISPR’ science: Newer genome editing tool shows promise in engineering human stem cells

DEEP BACKGROUND

Fascinating study linking genetic variation to language and linguistic variation.

Probing the deep history of human genes and language

2 hours ago by David Orenstein
Probing the deep history of human genes and language
Diversity of differences. Researchers analyzed distinct sounds — phonemes — in more than 2,000 languages around the world alongside genetic markers from more than 200 populations to uncover geographic patterns of how languages differ.
Brown University evolutionary biologist Sohini Ramachandran has joined with colleagues in publishing a sweeping analysis of genetic and linguistic patterns across the world’s populations. Among the findings is that geographic distance predicts differentiation in both language and genes.

Producing new insights into the evolution and development of around the globe is no easy task, but scientists can draw on multiple sources of data to do it. In a new study, Sohini Ramachandran and colleagues at Stanford University and University of Manitoba analyzed troves of data on genetics and distinct sounds in —phonemes—to discern important patterns.

Among the findings published in Proceedings of the National Academy of Sciences, is that genes and languages both vary more as geographic distance increases. The analysis showed there are distinct geographic patterns, or axes, of the greatest differences. The data also reflect how languages and genes evolve differently, for instance among isolated populations.

Ramachandran, assistant professor of ecology and evolutionary biology, discussed these and other insights with writer David Orenstein.

Why are language and genes sometimes combined in studies of populations?

Fields that study the human past, especially ancient human history, have to draw on multiple disciplines and lines of evidence in order to confirm and calibrate observed signatures in data, since we can’t truly know all events in human history. Because language is inherited ‘vertically’ [from parents to children] like genes, and also changes ‘horizontally’ based on contact among populations, many researchers in genetics interpret analyses of DNA from different populations in the context of the languages the study populations speak.

This kind of interdisciplinary work is what initially drew me to studying .

In this study what did you find was similar between languages and genes and what was different?

We saw that axes of differentiation in both our linguistic and genetic dataset corresponded, meaning that differences in both datasets of very different types of markers were geographically distributed quite similarly.

One very interesting contrast we saw between languages and genes had to do with isolated populations: an isolated population loses genetic diversity rapidly, as individuals marry within the ; in contrast, we saw a range of variation in linguistic markers for languages that are geographically isolated (have few neighboring languages). Some languages that are isolated lose complexity and others gain complexity and innovate new sounds. This makes me wonder whether contact among populations homogenizes their languages in some way so people can understand each other.

We found that linguistic markers do not hold signatures of the human expansion out of Africa, which is not surprising due to the rate at which languages changes and can be influenced by neighboring languages.

Tell us more about that difference between what genes and languages showed regarding human origins in Africa?

To be precise, genes tell us that the people living today with the most currently live in Southern Africa (like the San bushmen) and that modern humans emerged in Africa, but we don’t know where the geographic origin of our species was precisely based on genetic data. The language analysis did not reveal this African origin because language changes in a complex way, much differently from genes where we have a good sense of the mutation process. In my conversations with different linguists, including those at Brown who generously listened to me present our ideas multiple times, the rate at which language mutates, and which linguistic markers are more likely to change than others, seems to be an open question.

You found geographic axes, or directions, of difference in language and genetics. What might they tell us about human evolution and history?

These axes, which look for directions along which a dataset is most differentiated, tell us about axes along which humans likely did not migrate a great deal. For example, migration north/south in Africa would mean moving across climate regimes; we also know populations are quite different across latitudes in Europe and we see that for both our language datasets and genetic datasets.

What do your findings tell us about how we can use genes and language, either together or separately, for population studies?

We learn more from using both data types together and analyzing them using similar methods than we would have learned from either type alone. One signal we saw loud and clear in this study is how much geographic distance affected our ancestors’ and languages; geographic distance predicts differentiation in both data types, underscoring that there are still deep signatures of ancient migrations in our genomes and cultures today.

Explore further: Oceans apart: Study reveals insights into the evolution of languages

More information: “A comparison of worldwide phonemic and genetic variation in human populations,” by Nicole Creanza et al. PNAS, www.pnas.org/cgi/doi/10.1073/pnas.1424033112

Read more at: http://phys.org/news/2015-01-probing-deep-history-human-genes.html#jCp

There is but one way to advise – by example.

Homeschool on the Farm

Growing cotton, corn, and character

Duplicate My Success

How to Start a Blog From Scratch and Scale it to a Profitable Full-time Income on a Limited Budget

The Aramaic New Testament

Galilean Aramaic in the Context of Early Christianity

biblonia

A blog about books, words, history and the spaces in between. by Cristian Ispir

Submit your story logline and showcase it on this network. Or, submit to get your story made into a Video Pitch

Submit your logline pitch and we'll make sure it gets seen be 1000s. Over 1 million plus combined twitter and facebook followers

Jarrad Saul

Travel, Lifestyle and Occasionally Waffle

Mephit James Blog

From one GM to another.

Kristen Twardowski

A Writer's Workshop

The Public Domain Review

There is but one way to advise – by example.

Fantastic Maps

Fantasy maps and mapmaking tutorials by Jonathan Roberts

Matthew Zapruder

There is but one way to advise – by example.

Susie Day | children's books

books for kids about families, friendship, feelings and funny stuff

The Millions

There is but one way to advise – by example.

The Public Medievalist

The Middle Ages in the Modern World

There is but one way to advise – by example.

Chuck Wendig: Terribleminds

Hey Did You Know I Write Books

%d bloggers like this: