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The National Institutes of Child Health and Human Development awarded Phase I and Phase II Small Business Innovative Research Grants to develop The Visible Embryo. Initally designed to evaluate the internet as a teaching tool for first year medical students, The Visible Embryo is linked to over 600 educational institutions and is viewed by more than one million visitors each month.

Today, The Visible Embryo is linked to over 600 educational institutions and is viewed by more than 1 million visitors each month. The field of early embryology has grown to include the identification of the stem cell as not only critical to organogenesis in the embryo, but equally critical to organ function and repair in the adult human. The identification and understanding of genetic malfunction, inflammatory responses, and the progression in chronic disease, begins with a grounding in primary cellular and systemic functions manifested in the study of the early embryo.

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Pregnancy Timeline by SemestersFetal liver is producing blood cellsHead may position into pelvisBrain convolutions beginFull TermWhite fat begins to be madeWhite fat begins to be madeHead may position into pelvisImmune system beginningImmune system beginningPeriod of rapid brain growthBrain convolutions beginLungs begin to produce surfactantSensory brain waves begin to activateSensory brain waves begin to activateInner Ear Bones HardenBone marrow starts making blood cellsBone marrow starts making blood cellsBrown fat surrounds lymphatic systemFetal sexual organs visibleFinger and toe prints appearFinger and toe prints appearHeartbeat can be detectedHeartbeat can be detectedBasic Brain Structure in PlaceThe Appearance of SomitesFirst Detectable Brain WavesA Four Chambered HeartBeginning Cerebral HemispheresFemale Reproductive SystemEnd of Embryonic PeriodEnd of Embryonic PeriodFirst Thin Layer of Skin AppearsThird TrimesterSecond TrimesterFirst TrimesterFertilizationDevelopmental Timeline
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Home | Pregnancy Timeline | News Alerts |News Archive Sept 4, 2014

Everyone has an FMR1 gene.
But, repeating patterns of DNA (a “CGG repeat”) in FMR1 can lead to Fragile X syndrome.
Normally, about 30 repeats of CGG exist within a gene. Individuals with a "premutation,"
have 55-200 repeats. Persons with a full mutation have more than 200 CGG repeats.
More than 200 CGG repeats turn off the FMR1 gene by a process called Methylation —
which turns off the FMR1 gene, and no FMRP is produced. This is what causes Fragile X Syndrome.
More information on "premutation" can be found at the National Fragile X Foundation

 






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Single change in DNA could initiate fragile X

Researchers reveals how the alteration of a single nucleotide—the basic building block of DNA—could initiate fragile X syndrome, the most common inherited form of intellectual disability.

Fragile X syndrome is caused by a defect in a gene on the X chromosome called fragile X mental retardation 1 (FMR1).


Everyone has an FMR1 gene. But, about 1 in 230 women and 1 in 360 men carry a pre-mutation on their FMR1 gene, where a series of DNA repeats at one end of the gene make it slightly longer than normal.

These repeats are prone to increase even more when FMR1 is passed from mother to child. 


Researchers had previously identified a site on genes that initiates DNA replication — a site located near the FMR1 gene. 

However, this site is inactivated in fragile X. Inactivation changes the way the FMR1 gene is copied during cell division, which may lead to increases in DNA repeat errors within the FMR1 gene.

A DNA alteration in sequence located near the FMR1 gene has already been linked to an increased risk for repeat gene expansion, or increases in that repeat gene, in some people who carry gene premutations. In this current study, it was found that a particular single-nucleotide polymorphism (or SNP) is similar to the inactive replication switch found in fragile X.


Nucleotides in DNA include one of four bases — cytosine, thymine, adenine, or guanine.

Researchers found that normal cells had a thymine base at the SNP site with active replication of the gene error.

Fragile X cells, in contrast, had a cytosine base and are inactive.

It is believed the substitution of cytosine for thymine might inactivate DNA replication when the FMR1 gene is passed from mother to child, and increase the risk of the DNA error leading to fragile X syndrome.


Researchers also derived embryonic stem cells from mothers carrying the fragile X premutation. These cells had a thymine base and a normal replication pattern and showed no tendency to expand their repeat numbers over time.

All research was conducted at the Albert Einstein College of Medicine of Yeshiva University in New York, and appears in the Journal of Cell Biology.

Abstract
Fragile X syndrome (FXS) is caused by CGG repeat expansion that leads to FMR1 silencing. Women with a premutation allele are at risk of having a full mutation child with FXS. To investigate the mechanism of repeat expansion, we examined the relationship between a single-nucleotide polymorphism (SNP) variant that is linked to repeat expansion in haplogroup D and a replication origin located ∼53 kb upstream of the repeats. This origin is absent in FXS human embryonic stem cells (hESCs), which have the SNP variant C, but present in the nonaffected hESCs, which have a T variant. The SNP maps directly within the replication origin. Interestingly, premutation hESCs have a replication origin and the T variant similar to nonaffected hESCs. These results suggest that a T/C SNP located at a replication origin could contribute to the inactivation of this replication origin in FXS hESCs, leading to altered replication fork progression through the repeats, which could result in repeat expansion to the FXS full mutation.

Gerhardt, J., et al. 2014. J. Cell Biol. doi:10.1083/jcb.201404157

About The Journal of Cell Biology
The Journal of Cell Biology (JCB) is published by The Rockefeller University Press. All editorial decisions on manuscripts submitted are made by active scientists in conjunction with our in-house scientific editors. JCB content is posted to PubMed Central, where it is available to the public for free six months after publication. Authors retain copyright of their published works, and third parties may reuse the content for non-commercial purposes under a creative commons license. For more information, please visit http://www.jcb.org.

Research reported in this press release was supported by the National Institute of General Medical Sciences and National Institute of Child Health and Human Development of the National Institutes of Health, Empire State Stem Cell Fund, Starr Tri-Institutional Stem Cell Initiative, and Neurogenomics.

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