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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
CLICK ON weeks 0 - 40 and follow along every 2 weeks of fetal development
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Home | Pregnancy Timeline | News Alerts |News Archive Dec 12, 2013

 

A chromatin loop forms when an enhancer and a promoter, two widely separated elements in a DNA sequence, come into contact as they carry out gene activity.

Credit: The Children's Hospital of Philadelphia







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Gene switch may reverse sickle cell disease

In lab studies, researchers reprogram one gene and show proof-of-concept for a potential sickle cell therapy.

Hematology researchers at The Children's Hospital of Philadelphia (CHOP) have manipulated key biological events in adult blood cells to produce a form of hemoglobin normally absent after the newborn period. Because this fetal hemoglobin is unaffected by the genetic defect in sickle cell disease (SCD), the cell culture findings may open the door to a new therapy for the debilitating blood disorder.

"Our study shows the power of a technique called forced chromatin looping in reprogramming gene expression in blood-forming cells," said hematology researcher Jeremy W. Rupon, M.D., Ph.D., of The Children's Hospital of Philadelphia. "If we can translate this approach to humans, we may enable new treatment options for patients."

Rupon presented the team's findings today at a press conference during the annual meeting of the American Society of Hematology (ASH) in New Orleans. Rupon worked in collaboration with a former postdoctoral fellow, Wulan Deng, Ph.D., in the laboratory of Gerd Blobel, M.D., Ph.D.

Hematologists have long sought to reactivate fetal hemoglobin as a treatment for children and adults with SCD, the painful, sometimes life-threatening genetic disorder that deforms red blood cells and disrupts normal circulation.


In the normal course of development, a biological switch flips during the production of hemoglobin, the oxygen-carrying component of red blood cells. Regulatory elements in DNA shift the body from producing the fetal form of hemoglobin to producing the adult form instead. This transition occurs shortly after birth.

When patients with SCD undergo this transition, their inherited gene mutation distorts adult hemoglobin, forcing red blood cells to assume a sickled shape.

In the current study, Rupon and Blobel reprogrammed gene expression to reverse the biological switch, causing cells to resume producing fetal hemoglobin, which is not affected by the SCD mutation, and produces normally shaped red blood cells.


The scientists built on previous work by Blobel's team showing that chromatin looping, a tightly regulated interaction between widely separated DNA sequences, drives gene transcription—the conversion of DNA code into RNA messages to carry out biological processes.


In the current study, the researchers used a genetically engineered zinc finger (ZF) protein, which they custom-designed to latch onto a specific DNA site carrying the code for fetal hemoglobin. They attached the ZF to another protein that forced a chromatin loop to form.

The loop then activated gene expression that produced embryonic hemoglobin in blood-forming cells from adult mice. The team obtained similar results in human adult red blood cells, forcing the cells to produce fetal hemoglobin.


Rupon and Blobel will continue investigations aimed at moving their research toward clinical application. Rupon added that the approach may also prove useful in treating other diseases of hemoglobin, such as thalassemia.

From presentation:
In this study, investigators sought to direct this chromatin loop away from the adult globin genes and instead turn on fetal globin genes to stimulate the production of normal fetal hemoglobin. Elevated levels of fetal hemoglobin have long been known to ameliorate the clinical course of SCD and some forms of β-thalassemia. Using synthetic proteins called zinc fingers (ZFs), investigators redirected the chromatin loop to activate embryonic globin genes in mice and fetal globin genes in humans. Specifically, the researchers designed ZFs that would bind to the part of the LCR that initiates embryonic gene transcription, fused them to protein elements previously known to be involved in chromatin loop formation, and introduced them into an adult mouse red blood cell line that normally produces nearly 100 percent adult β globin. This led to marked activation of embryonic globin production that was dependent on chromatin looping. The authors then employed the same approach in human cells, where they used ZFs to create a chromatin loop connecting the fetal globin genes with the LCR. This led to a striking increase in fetal globin, accounting for nearly 90 percent of total globin production.

Financial support for this study came from the National Institutes of Health (grants 5R37DK058044 and RO1HL119479-01) and a fellowship award from the American Heart Association. Wulan Deng, Ph.D., a former member of Blobel's lab, is a co-author of the study. Other co-authors include scientists from Sangamo Biosciences, which designed the zinc finger proteins. In addition to his position at Children's Hospital, Blobel is also at the Perelman School of Medicine at the University of Pennsylvania.

"Using Forced Chromatin Looping to Overcome Developmental Silencing of Embryonic and Fetal beta-Type Globin Genes in Adult Erythroid Cells"

--Abstract 59341, presented Sun., Dec. 8, 2013, 11 a.m. CT; Press Conference to occur in the ASH Press Room, Rm. 356-357, Ernest N. Morial Convention Center--

About The Children's Hospital of Philadelphia: The Children's Hospital of Philadelphia was founded in 1855 as the nation's first pediatric hospital. Through its long-standing commitment to providing exceptional patient care, training new generations of pediatric healthcare professionals and pioneering major research initiatives, Children's Hospital has fostered many discoveries that have benefited children worldwide. Its pediatric research program receives the highest amount of National Institutes of Health funding among all U.S. children's hospitals. In addition, its unique family-centered care and public service programs have brought the 535-bed hospital recognition as a leading advocate for children and adolescents. For more information, visit http://www.chop.edu.