Zoi-Sci

Imagine a “biocomputer” inside your body monitoring what’s going on inside, identifying the unhealthy cells, and even releasing treatment dose. Thanks to researchers at Harvard and Princeton Universities, one day this may come true!!

Scientists have devised a tiny “biocomputer”, which can one day be implanted in human cells to monitor their activities and characteristics. Composed of only genetic materials, these “molecular doctors” hold the promise of revolutionizing medicine by targeting only diseased cells or tissues, leaving healthy ones completely unaffected.

These “biocomputers” are designed to detect anything from the presence of a mutated gene to the activity of genes within the cell using Boolean logic. To create a “molecular computer” capable of making decisions is a big challenge in itself and getting them to work in human cells is likely to be even trickier.

Primary goal involves injecting human cells with DNA to determine if a cell is cancerous or otherwise diseased. If disease is detected, the DNA might trigger an accurate treatment dose in response. As of now, researchers are in the testing stage of turning DNA into versatile computers (published online at Nature Biotechnology very recently).

Cells have short interfering RNA (siRNA) molecules which recognize corresponding DNA sequences in genes, causing them to shut down. This system is based on the process RNA interference (RNAi).

Reference:

• Sciam
• Harvard press release
• Physorg
• Image via Sciam

Twins intermediate between identical and fraternal discovered

A person who is a chimera has two or more genetically different cells coming from different zygotes. A chimera can be formed in either of the following two ways:

1. From four parent cells – Two fertilized eggs or early embryos fuse together
2. From three parent cells – A fertilized egg is fused with an unfertilized egg or a fertilized egg is fused with an extra sperm

We all know that there are identical twins and non-identical or fraternal twins. Now an instance of ’semi-identical’ twins has come up.

This is the first time that a case of ’semi-identical’ twins has been reported. This is a case of three-parent cells fusion in which two sperm cells fuse with a single egg which makes the twins chimeras. So, here the twins are identical through their mother’s side, but share only half their genes on their father’s side.

According to geneticist Vivienne Souter, of the Banner Good Samaritan Medical Center in Phoenix, Arizona:

“Their similarity is somewhere between identical and fraternal twins.”

This case came to the notice of Souter and her colleagues while they were investigating one of the twins’ genetic makeup, who was born with ambiguous genitalia.

Formation of chimera is a rare occurrence in itself. This ‘double-fertilization’ due to fusion of a single egg by two sperms is thought to happen in about only 1% of human conceptions. But, the subsequent twinning of chimeras may be the rarest of the rare.

According to news@nature

“Their existence and discovery relies on three unusual, and possibly unlinked, events: first, that an egg fertilized by two sperm develops into a viable embryo; second, that this embryo splits to form twins; and third, that the children come to the attention of science.”

The twins were conceived and born normally and their growth and mental abilities appear normal. It is really astonishing to hear that the twins still came out to be healthy after being conceived through this rare, complicated and almost impossible process.

15 per cent-human sheep

Now another instance of Chimera…this time – closer to the origin of the word ‘Chimera’ which comes from a creature in Greek mythology that had body parts from a goat, a lion and a serpent. Well not exactly…

Here goes the way mythological character looks like

Scientists have successfully created a human – sheep chimera, which has the body of a sheep and partial human organs for the first time

The purpose of the creation of these chimeras, which has 15 per cent human cells and 85 percent animal cells, is to create organs which contain large proportion of human cells for subsequent transplantation into human bodies.

This technique, perfected by Professor Esmail Zanjani, of the University of Nevada, involves injection of adult human cells into foetus of a sheep.

Though this human-sheep chimera has been created with an intention of saving human lives, it is likely to meet criticisms about scientist playing with natural creation and also the possibility of introducing silent animal viruses in human body (which are harmless for animal, but may be threat for humans).

Dr Patrick Dixon, an international lecturer on biological trends, warned:

“Many silent viruses could create a biological nightmare in humans. Mutant animal viruses are a real threat, as we have seen with HIV.”

There is also a fear that this process could end up creating a hybrid with the features and characteristics of both man and sheep.

But Prof Zanjani refuted this :

“Transplanting the cells into foetal sheep at this early stage does not result in fusion at all.”

Read more about this here.

Sources (including image source):

Wikipedia
Nature
Dailymail

Ethnic factors play a key role in determining infertility in men, a study of 560 infertile men by scientists has revealed. Some causative factors which cause infertility elsewhere do not affect Indian men, the study found. The study was conducted by Dr K. Thangaraj of the Centre for Cellular and Molecular Biology, Hyderabad, and B.N. Chakra-varthi of the Institute of Reproductive Medicine, Kolkata.

About 15 per cent of couples are infertile due to various causes. Of this, male and female factors contribute 50 per cent each. It has been estimated that genetic/ethnic factors play a role in about 10 per cent of male infertility. The ’male’ Y chromosome consists of three azoospermia factor regions (AZFa, AZFb and AZFc). A large number of genes in these regions exist in multiple copies. In addition, autosomes and X chromosomes also have genes responsible for male fertility.

The initial analysis of 560 infertile men revealed that the deletions on Y chromosome were responsible for about 12 per cent of them. To find out the molecular cause for the remaining 88 per cent of the men, the team analysed samples with other potential genes. Four copies of ‘DAZ gene’ are located in AZFc region. Deletion of one or more copies of DAZ gene was found in 16 per cent of the infertile men.

But DAZ copy deletion was found to be significant only in 5.5 per cent of the infertile men. Deletion of another gene, CDY, was found in 5.8 per cent. Analysis of the autosomal homologue of the DAZ, which was found to be associated with make infertility in some populations, is not found to be associated with male infertility in Indians. The scientists suggest that the genetic and ethnic factors play a major role in male infertility.

Male infertility: No Evidence of Involvement of Androgen Receptor Gene among Indian Men

ABSTRACT

Spermatogenesis is collaborately controlled by testosterone (T) and follicle stimulating hormone (FSH). Testosterone and its immediate metabolite, dihydrotestosterone (DHT) affect their roles through androgen receptor (AR). Mutations in AR gene have been shown to cause partial to complete androgen insensitivity or infertility in otherwise normal males. Dependence of germ cells upon Sertoli and Leydig cells for their differentiation into sperms, and deletion studies of AR gene in animal models indicate a direct or indirect role of AR gene in spermatogenesis. Although few studies worldwide have reported AR mutations in male infertility, no similar study has been conducted on Indian populations. Therefore, we undertook this study to look at the contribution of AR mutations in male infertility among Indian men. We have sequenced complete coding region of AR gene in a total of 399 infertile samples, comprising 277 azoospermic, 100 oligozoospermic and 22 oligoteratozoospermic samples. A total of 100 healthy males with proven fertility and same ethnicity served as controls. Sequence analysis revealed no mutation in any of these samples. Our study suggests that the mutations in AR gene are less likely to cause azoospermia and oligozoospermia, however, it was difficult to rule out in oligoteratozoospermia as the sample size was small.

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Scientific American: Are Scientists Closer to Discovering a Fountain of Youth?
International study kicked off by a prematurely aging boy provides insight into the mechanisms behind growing older

The case of a 15-year-old Afghan boy with a rare genetic condition that caused him to age rapidly may help scientists unlock the mysteries how and why we age, bringing them closer to finding a way to halt or dramatically slow the aging process.

Physicians discovered that the boy, admitted to a Dutch hospital in the 1990s suffering from symptoms including hypertension, hearing and vision loss, kidney failure, anemia and sensitivity to light, had a mutation in a key gene responsible for the enzyme that is essential to the repair of DNA damage in cells. The genetic flaw caused him to age prematurely and die essentially of old age before completing puberty.

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Among the many genes packed into each cell of our body, those that get turned on, or expressed, are the ones that make us who we are. Certain proteins do the job of regulating gene expression by clasping onto key spots of DNA — the nucleic acid that contains the genetic instructions.

How does the protein recognize a particular binding site? Structural changes in both the protein and DNA, sometimes with the DNA within the complex kinked or sharply bent, allow for the specific contacts needed for a tight DNA-protein fit.

Scientists think DNA is largely passive in this genetic tango. But new findings by Anjum Ansari, associate professor of biophysics at the University of Illinois at Chicago, suggest DNA may not be the wallflower that many had assumed.

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It may look like mistletoe wrapped around a flexible candy cane. But this molecular model shows how some proteins form loops in DNA when they chemically attach, or bind, at separate sites to the double-helical molecule that carries life’s genetic blueprint.

Biologists have discovered that the physical manifestation of DNA loops are a consequence of many biochemical processes in the cell, such as the regulation of gene expression. In other words, these loops indicate the presence of enzymes or other proteins that are turned on. Now physicists at the University of California, San Diego have discovered that stretching the DNA molecule can also turn off the proteins known to cause loops in DNA.

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The dance of the chromosomes during cell division, first described in the late 1800s and familiar to all high-school students from movies shown in biology classes, has long fascinated biologists. However, the molecular nature of a key component of cell division, the “chromosome-spindle” connection, which is critical for the inheritance of genetic information as cells divide, has remained elusive.

Researchers at the University of California, San Diego (UCSD) School of Medicine and the Ludwig Institute for Cancer Research have identified a protein group that forms the chromosome-spindle connection involved in pulling apart the two replicas of the duplicated genome during cell division. They have also identified a separate protein complex that helps the cell discriminate between correct and incorrect spindle connections, and shuts down the pulling process when the connections are incorrect to ensure that each new cell has a complete set of chromosomes.

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More than a decade of searching for factors that make the common parasite Toxoplasma gondii dangerous to humans has pinned 90 percent of the blame on just one of the parasite’s approximately 6,000 genes.

The finding, reported in this week’s issue of Science by researchers at Washington University School of Medicine in St. Louis and elsewhere, should make it easier to identify the parasite’s most virulent strains and treat them. The results suggest that when a more harmful strain of T. gondii appears, approximately 90 percent of the time it will have a different form of the virulence gene than that found in the more benign strains of the parasite.

ROP18, the T. gondii virulence gene identified by researchers, makes a protein that belongs to a class of signaling factors known as kinases that are ubiquitous in human biology.

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Researchers have not yet identified the exact cause of Autism. But certain findings strongly indicate that risk of Autism is not due to a single gene but due to multi-gene interaction and environmental factors.
The identification of a new gene linked to autism may help in knowing more about this mysterious condition.

Researchers identify gene linked to autism from PhysOrg.com
French researchers have discovered a new gene linked to autism, a mental disability which prevents sufferers from communicating and forming relationships normally and whose causes are unknown. The study, published Sunday online by Nature Genetics journal, found that all of five autistic children studied had anomalies in the SHANK3 gene, responsible for making the connections in the brain necessary for language development.

The most distinctive symptoms of autism are problems with communication, forming relationships and developing strong obsessional traits.

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