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Can Calico Cats Be Male?
BY DR. MARTY BECKER | MAY 17, 2013

Q. Is it true that male cats can’t be calico and female cats can’t be orange tabbies?
A. Not true in either case. But male calicos are rare: Only one out of every 3,000 calico cats is male, according to a study by the College of Veterinary Medicine at the University of Missouri.
The gene that governs how the orange color in cats displays is on the X chromosome. Any cat, male or female, can be orange, but in males the color is nearly always expressed in the tabby (striped) pattern, sometimes called a ginger tom. Females can be orange tabby, calico or tortoiseshell. (The last two are genetically similar, except the calico has patches of white, orange and brown or black, and the tortie’s colors are orange and brown or black swirled together.)
Because the orange is divided among tabbies, torties or calicoes in females, there are fewer of each type. And because orange is almost always associated with tabby in males, it seems as if there are more orange males than orange females. That’s probably the case, but no one’s counting.
Here’s where it really gets interesting. Female cats have two X chromosomes, while male cats have an X and a Y chromosome. For a cat to be a calico or tortoiseshell, the animal must have two X chromosomes, which means the kitty is going to be female the vast majority of the time. When the calico pattern exists in a male, it’s because the cat has three sex chromosomes: two X, one Y (male).
The XXY combination is a genetic rarity that occasionally shows up in cats (people, too). And if both X chromosomes carry the calico blueprint, you’re looking at one rare cat: a male calico.
Such XXY animals are called Klinefelter males, after the doctor who first described the condition. If you have a male calico and think you can make money breeding him, you probably won’t. Though lovely, the cats are usually sterile.
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Can Calico Cats Be Male?

Sexual Maturity in Girls Influenced by ‘Imprinted’ Genes from Different Parents
How long does it take a girl to reach maturity? It depends a lot on their genes. It turns outs that the age at which girls reach sexual maturity is influenced by “imprinted genes,” which are a small sub-set of genes whose activity differs depending on which parent passes on that gene.
"Normally, our inherited physical characteristics reflect a roughly average combination of our parents’ genomes, but imprinted genes place unequal weight on the influence of either the mother’s or the father’s genes," said John Perry, one of the researchers, in a news release. ”Our findings imply that in a family, one parent may more profoundly affect puberty timing in their daughters than the other parent.”
In order to better understand puberty in women, the researchers examined more than 180,000 women. More specifically, they identified 123 genetic variations that were associated with the timing of when girls experienced their first menstrual cycle by analyzing the DNA of 182,416 women of European descent.
The activity of imprinted genes differs depending on which parent the gene is inherited from. For example, some genes are only active when inherited from the mother, while others are only active when inherited from the father. Both types of these imprinted genes were identified as determining puberty timing in girls. This suggests a possible biological conflict between the parents of their child’s rate of development.
"We knew that some imprinted genes control antenatal growth and development-but there is increasing interest in the possibility that imprinted genes may also control childhood maturation and later life outcomes, including disease risks," said Perry.
The findings reveal that while lifestyle factors do play a role in puberty, there’s also a wide and complex network of genetic factors. The research could help scientists find out why early puberty in girls is linked to higher risks of developing diabetes, heart disease and breast cancer later in life.
The findings are published in the journal Nature.
source 

Sexual Maturity in Girls Influenced by ‘Imprinted’ Genes from Different Parents

How long does it take a girl to reach maturity? It depends a lot on their genes. It turns outs that the age at which girls reach sexual maturity is influenced by “imprinted genes,” which are a small sub-set of genes whose activity differs depending on which parent passes on that gene.

"Normally, our inherited physical characteristics reflect a roughly average combination of our parents’ genomes, but imprinted genes place unequal weight on the influence of either the mother’s or the father’s genes," said John Perry, one of the researchers, in a news release. ”Our findings imply that in a family, one parent may more profoundly affect puberty timing in their daughters than the other parent.”

In order to better understand puberty in women, the researchers examined more than 180,000 women. More specifically, they identified 123 genetic variations that were associated with the timing of when girls experienced their first menstrual cycle by analyzing the DNA of 182,416 women of European descent.

The activity of imprinted genes differs depending on which parent the gene is inherited from. For example, some genes are only active when inherited from the mother, while others are only active when inherited from the father. Both types of these imprinted genes were identified as determining puberty timing in girls. This suggests a possible biological conflict between the parents of their child’s rate of development.

"We knew that some imprinted genes control antenatal growth and development-but there is increasing interest in the possibility that imprinted genes may also control childhood maturation and later life outcomes, including disease risks," said Perry.

The findings reveal that while lifestyle factors do play a role in puberty, there’s also a wide and complex network of genetic factors. The research could help scientists find out why early puberty in girls is linked to higher risks of developing diabetes, heart disease and breast cancer later in life.

The findings are published in the journal Nature.

source 

Red Fish, Blue Fish: Where The Fish Flesh Rainbow Comes From

Evolution is awesome!  A native group of people living on the Soloman Islands northeast of Australia called Melanesians is famous for their beautiful dark skin and naturally blonde hair. The odd combination has got scientists wondering about how such a color combo develops over time. According to the Global Financial Newswires, many scientists have long thought that their blonde hair was a result of a diet high in fish, perhaps bleaching by the sun and salt water, or a reminder of the island’s historic relations with people of European descent.In fact, the blonde Melanesians have blonde that is unique solely to them. According to the study in which scientists compared 43 blonde hair islanders to 42 dark hair islanders, blonde Melanesians have a variant of a native gene called TYRP1 that plays an important role in the melanin biosynthetic pathway. This variant is completely separate from what causes blonde hair in Europeans, and doesn’t even exist in the European genetic set.What’s truly beautiful in this fascinating discovery, as so perfectly stated by the study author Sean Myles, a geneticist at Nova Scotia Agricultural College, is that “it’s a great example of convergent evolution, where the same outcome is brought about by completely different means.”Found on http://tinyurl.com/6u8kwhl
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Evolution is awesome!  A native group of people living on the Soloman Islands northeast of Australia called Melanesians is famous for their beautiful dark skin and naturally blonde hair. 

The odd combination has got scientists wondering about how such a color combo develops over time. According to the Global Financial Newswires, many scientists have long thought that their blonde hair was a result of a diet high in fish, perhaps bleaching by the sun and salt water, or a reminder of the island’s historic relations with people of European descent.

In fact, the blonde Melanesians have blonde that is unique solely to them. According to the study in which scientists compared 43 blonde hair islanders to 42 dark hair islanders, blonde Melanesians have a variant of a native gene called TYRP1 that plays an important role in the melanin biosynthetic pathway. This variant is completely separate from what causes blonde hair in Europeans, and doesn’t even exist in the European genetic set.

What’s truly beautiful in this fascinating discovery, as so perfectly stated by the study author Sean Myles, a geneticist at Nova Scotia Agricultural College, is that “it’s a great example of convergent evolution, where the same outcome is brought about by completely different means.”

Found on http://tinyurl.com/6u8kwhl

source 

What Are The Odds? – Kermode Bear

The Spirit Bear is actually a white Black Bear, which sounds funny and incredibly contradictory but it is the truth. They are not albino and as such don’t have the pink eyes that is normally associated with albino animals, rather the colour of their fur is a result of two recessive genes being expressed. It is believed that 1 out of 10 Black Bears carry this recessive “white-coat” gene, so in theory, they should be able to exist anywhere that Black Bears live. Interestingly enough, the main population of Kermode Bears can be found on the islands off the coast of British Columbia, Canada in a temperate rainforest appropriately named the Great Bear Rainforest. The population of Spirit Bears is most likely greatest in this area as a result of conservation efforts of the First Nation tribes. These groups valued the Kermode Bear and as such didn’t hunt or trap this beautiful creature. As a result it is believed that the population of the Spirit Bear is between 400-1000 individuals in this area. How is that for proof that animal conservation can truly help a species (or sub-species) survive.

source for above text

I really dislike the way this and most articles are written about the Kermode Bear so I am also going to link in the well known Nat Geo article for a full understanding.

ANATOMY OF OUR GENES: The Human Body

The human body is made of some 50 trillion to 100 trillion cells, which form the basic units of life and combine to form more complex tissues and organs. Inside each cell, genes make up a “blueprint” for protein production that determines how the cell will function. Genes also determine physical characteristics or traits. The complete set of some 20,000 to 25,000 genes is called the genome. Only a tiny fraction of the total genome sets the human body apart from those of other animals.

Most cells have a similar basic structure. An outer layer, called the cell membrane, contains fluid called cytoplasm. Within the cytoplasm are many different specialized “little organs” called organelles. The most important of these is the nucleus, which controls the cell and houses the genetic material in structures called chromosomes. Another type of organelle is mitochondrion. These “cellular power plants” have their own genome and do not recombine during reproduction.

Chromosomes

Chromosomes carry hereditary, genetic information in long strings of DNA called genes. Humans have 22 numbered pairs of chromosomes and a single pair of sex chromosomes—XX in females and XY in males. Each chromosomal pair includes one inherited from the father and one from the mother. If unwound, the microscopic DNA strands in one cell’s nucleus would stretch to over six feet (two meters) in length.

DNA

DNA (deoxyribonucleic acid) is the set of genetic instructions for creating an organism. DNA molecules are shaped like a spiral staircase called a double helix. Each stair is composed of the DNA bases A, C, T, and G. Some segments of these bases contain sequences, like A-T-C-C-G-A-A-C-T-A-G, which constitute individual genes. Genes determine which proteins individual cells will manufacture, and thus what function particular cells will perform. 

read more, photos and info from Nat Geo

Albinism is a genetic condition also called achromia, achromasia, or achromatosis. It is characterized by a deficit in the production in melanin and by the partial or complete absence of pigment in the skin, hair and eyes. This hereditary disease can be found in humans (affecting all races), mammals, birds, fish, reptiles and amphibians. 

Even though it is a hereditary condition, in most cases, there’s no family history of albinism.

People with albinism often have vision problems and are susceptible to sunburns and skin cancers if they do not protect themselves from direct sunlight. 

According to The National Organization for Albinism and Hypopigmentation, one in every 17,000 people in the United States has some type of albinism.

What are the signs and symptoms of albinism?

Since birth, people with albinism have little or no pigmentation in their eyes, skin and hair (oculocutaneous albinism) or sometimes in the eyes alone (ocular albinism). 


The degree of pigmentation varies. Some people gain a little pigmentation in their hair or eyes with age. Some develop pigmented freckles on their skin. An individual with complete absence of melanin is called an albino. One with only a small amount of melanin is described as albinoid.

People with albinism are very pale with fair hair and very light eyes. In some people, the eyes appear red or purple, depending on the amount of pigment. This can happen because the iris actually has very little color. The eyes appear pink or red because the blood vessels inside of the eye show through the iris. 

A person with albinism is generally as healthy as the rest of the population. However, problems with vision and skin are particularly common. 

Vision Problems. Vision problems in albinism result from abnormal development of the retina and abnormal patterns of nerve connections between the eye and the brain. Most people with albinism have problems with their eyesight; many have low vision. Lack of pigment in the eyes results in problems with eyesight, both related and unrelated to photosensitivity. This sensitivity generally leads to discomfort in bright light. 

Skin problems. The dark pigment - melanin - helps protect the skin from the sun’s ultraviolet radiation. People with albinism lack this pigment; their skin can burn more easily from overexposure. They need to take precautions to avoid damage to the skin caused by the sun; this means applying sunscreen lotions, and wearing hats and sun-protective clothing.

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photos of animals from Nat Geo

photos of people from Gustavo Lacerda’s photo project on Albinism  


Big Pic: A Fruit Fly Born In Outer Space


Something seems a little off here…

By 


Francie Diep


This is a fruit fly, raised in space. Space was not directly what made it furred all over with white, but indirectly it was. The white stuff is fungus, and the fly grew it because after hatching and growing to adulthood in space, it didn’t fight off a fungal infection the way a healthy fly that had grown up on Earth would.
The image comes from the research of a team of biologists from several U.S. institutions. Observations of astronauts and studies done in human immune cells have shown that space weakens the immune system. This U.S. team wanted to learn more about what was happening at a cellular level. Their little spacefaring flies taught them that low gravity shuts off an important component of the fly immune system—one that has a human counterpart.  
Their findings gave them some starting ideas about why people also have compromised immunity after spending time in space, they wrote in a paper they published today in the journal PLOS ONE. One experiment they performed in hypergravity—created for the flies using a centrifuge in a lab on Earth—also suggested exposure to gravity could prevent the immune effects of space.
The team sent fruit fly eggs to space aboard the space shuttle Discovery. (Fun fact: These were the first flies to go into space in the name of immunology.) The eggs spent 12 days in space, during which time they hatched, crawled around a bit as larva, and became adult flies. Then they came back down to Earth, where biologists infected them with one of two things, either E. colibacteria or a fungus called Beauveria bassiana. (I survived space and all I got was a fungal infection.)
The space flies’ immune system fought off the E. coli, but not the Beauveria bassiana fungus. Meanwhile, similar control flies raised on Earth fought off both infections.
To figure out why the space flies had trouble with the fungus, the scientists analyzed all of the flies’ genes. Both the space flies and the Earth flies were born with the same genes, but exactly which of those genes turned on and went to work differed between them. In Earth flies, the genes associated with their immune systems kicked into high gear after they got infected with the fungus. Among other genes, Earth flies activated something called the Toll signaling pathway, which scientists have long known flies use to fight off fungi. Humans have Toll-like genes, too, and they also work in immunity.
The space flies reacted differently from their stay-at-home siblings. They turned on some immunity genes after encountering Beauveria bassiana, so it’s not like they were totally helpless. But they didn’t use all of the genes the Earth flies used, and they didn’t turn up their Toll pathway genes. In their paper, the biologists called their spacefaring flies “severely immunocompromised.”
Strangely, when the biologists raised flies in a centrifuge to simulate higher-than-Earth gravity, they were more likely to survive a fungal infection than normal Earth flies.
The science team offered some hypotheses about what could be happening that would alter what genes flies activate, depending on the gravity they’re exposed to. The hypotheses are testable, the team noted, although the team didn’t do that for this paper. The next step should be to send fruit flies to the International Space Station, the biologists wrote, where the little bugs can spend longer in space.
from Popsci

Big Pic: A Fruit Fly Born In Outer Space

Something seems a little off here…




The gene, Lin28a, is being dubbed the “Wolverine” or “Fountain of Youth” gene. It’s usually only produced in developing embryos, but when switched on in adult mice it causes them to grow hair faster and repair bone, cartilage, skin and other soft tissues almost completely. Lin28a works by boosting metabolism in mitochondria, a discovery that could lead to regenerative treatments in humans.
Read more: http://bit.ly/1c2M1xy via Nature. Image: 20TH CENTURY FOX/REX FEATURES

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The gene, Lin28a, is being dubbed the “Wolverine” or “Fountain of Youth” gene. It’s usually only produced in developing embryos, but when switched on in adult mice it causes them to grow hair faster and repair bone, cartilage, skin and other soft tissues almost completely. Lin28a works by boosting metabolism in mitochondria, a discovery that could lead to regenerative treatments in humans.

Read more: http://bit.ly/1c2M1xy via Nature. Image: 20TH CENTURY FOX/REX FEATURES

Aniridia is a genetic condition that affects people at birth. The term “aniridia” literally means “without iris” (the colored part of the eye), which is generally the first indication that an individual has aniridia.  A person who has aniridia is born without a fully developed iris. The name ‘aniridia’ is somewhat misleading because aniridia is a panocular condition, meaning it usually affects other components of the anatomy of the eye in addition to the iris.

Actually, the lack of the iris is the least of the ocular problems associated with aniridia. Aniridia can affect the entire anatomy – the cornea, the fovea or retina, as well as the lens.  As a result, ocular conditions can include glaucoma, foveal hypoplasia, nystagmus, strabismus, dry eye, corneal degeneration, and cataracts. Most people with aniridia have at least one of these associated ocular conditions that impact their vision.

Aniridia is a rare eye condition, affecting approximately 1 in 60,000 births.  However, the ocular problems associated with aniridia mentioned above are quite common.  What is rare is to have all of these conditions present in one individual.

Although people with aniridia always have vision problems, the degree varies greatly and is dependent upon which complications, in addition to the lack of iris, an individual has.  Generally, individuals with aniridia have a visual acuity measurement between 20/80 and 20/200.  Some are legally blind, while others have vision good enough to drive a car.  Most individuals with aniridia read without using Braille, especially in today’s technically advanced environment of e-Readers.

It is important to note that some of the conditions related to aniridia are non-degenerative (meaning they do not get worse over time) and others are degenerative.  Conditions that can degenerate the vision of an individual with aniridia include corneal keratopathy, glaucoma, and cataracts.  For more information on these conditions and treatments, please refer to the menu on the right ‘Aniridia’s Impact on Vision’ under the ‘Learn More’ heading.

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