Welcome to The Visible Embryo

Home-- -History-- -Bibliography- -Pregnancy Timeline- --Prescription Drugs in Pregnancy- -- Pregnancy Calculator- --Female Reproductive System- -Contact
 

Welcome to The Visible Embryo, a comprehensive educational resource on human development from conception to birth.

The Visible Embryo provides visual references for changes in fetal development throughout pregnancy and can be navigated via fetal development or maternal changes.

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.

WHO International Clinical Trials Registry Platform


The World Health Organization (WHO) has created a new Web site to help researchers, doctors and
patients obtain reliable information on high-quality clinical trials. Now you can go to one website and search all registers to identify clinical trial research underway around the world!



Home

History

Bibliography

Pregnancy Timeline

Prescription Drug Effects on Pregnancy

Pregnancy Calculator

Female Reproductive System

Contact The Visible Embryo

News Alerts Archive

Disclaimer: The Visible Embryo web site is provided for your general information only. The information contained on this site should not be treated as a substitute for medical, legal or other professional advice. Neither is The Visible Embryo responsible or liable for the contents of any websites of third parties which are listed on this site.
Content protected under a Creative Commons License.

No dirivative works may be made or used for commercial purposes.

Return To Top Of Page
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
Google Search artcles published since 2007
 
 

Home | Pregnancy Timeline | News Alerts |News Archive Sep 9, 2013

 

homlogous recombination

Chromosoma reaangement as DNA is being synthesized into protein.,






DNA damage chart



Signal Transduction: sending an SOS to repair DNA

WHO Child Growth Charts

 

 

 

Two paths where chromosomes rearrange and fail

Discovery provides target to potentially halt the process, prevent cancers.

Biologists reported today in Nature that they have identified two pathways through which chromosomes are rearranged in mammalian cells. These types of changes are associated with some cancers and inherited disorders in people.

"Our finding provides a target to prevent these rearrangements, so we could conceivably prevent cancer in some high-risk people," said senior author Edward P. (Paul) Hasty, D.V.M., of the School of Medicine at The University of Texas Health Science Center at San Antonio. Partial funding came from the Cancer Therapy & Research Center at the UT Health Science Center San Antonio.


The two pathways rearrange chromosomes by recombining DNA repeats that are naturally found in the genome, Dr. Hasty said.

DNA, the chemical substance of genes, denatures and replicates during cell division and other processes. Repeats are sequences of DNA that are duplicated.


Both pathways are important for the synthesis of DNA. "Therefore, we propose that chromosomal rearrangements occur as DNA is being synthesized," Dr. Hasty said.


The experiments were conducted with mouse embryonic stem cells grown in tissue culture.

The team measured the incidence of DNA repeats recombining in normal cells. This is called "repeat fusion."

The scientists then looked for incidence of repeat fusion in cells affected by several genetic mutations. This analysis identified the two pathways and showed large, complicated rearrangements that involved DNA repeats on multiple chromosomes.


During cell division, DNA is coiled into pairs of threadlike structures called the chromosomes. Each human cell has 22 numbered pairs of chromosomes called autosomes. The sex chromosomes are the 23rd pair in cells and determine a person's gender. Females have two X chromosomes, while males have an X and a Y chromosome.

"We hope the new findings will help us better understand the mechanisms that cause chromosomal instability, which causes some cancers in people," Dr. Hasty said.

At the Health Science Center, Dr. Hasty is a professor in the Department of Molecular Medicine, has a laboratory at the UT Institute of Biotechnology, and is a faculty member of the Barshop Institute for Longevity and Aging Studies.

Abstract
Replication fork maintenance pathways preserve chromosomes, but their faulty application at nonallelic repeats could generate rearrangements causing cancer, genomic disorders and speciation1, 2, 3. Potential causal mechanisms are homologous recombination and error-free postreplication repair (EF-PRR). Homologous recombination repairs damage-induced DNA double-strand breaks (DSBs) and single-ended DSBs within replication. To facilitate homologous recombination, the recombinase RAD51 and mediator BRCA2 form a filament on the 3′ DNA strand at a break to enable annealing to the complementary sister chromatid4 while the RecQ helicase, BLM (Bloom syndrome mutated) suppresses crossing over to prevent recombination5. Homologous recombination also stabilizes6, 7 and restarts8, 9 replication forks without a DSB10, 11. EF-PRR bypasses DNA incongruities that impede replication by ubiquitinating PCNA (proliferating cell nuclear antigen) using the RAD6–RAD18 and UBC13–MMS2–RAD5 ubiquitin ligase complexes12. Some components are common to both homologous recombination and EF-PRR such as RAD51 and RAD1813, 14. Here we delineate two pathways that spontaneously fuse inverted repeats to generate unstable chromosomal rearrangements in wild-type mouse embryonic stem (ES) cells. Gamma-radiation induced a BLM-regulated pathway that selectively fused identical, but not mismatched, repeats. By contrast, ultraviolet light induced a RAD18-dependent pathway that efficiently fused mismatched repeats. Furthermore, TREX2 (a 3′5′ exonuclease) suppressed identical repeat fusion but enhanced mismatched repeat fusion, clearly separating these pathways. TREX2 associated with UBC13 and enhanced PCNA ubiquitination in response to ultraviolet light, consistent with it being a novel member of EF-PRR. RAD18 and TREX2 also suppressed replication fork stalling in response to nucleotide depletion. Interestingly, replication fork stalling induced fusion for identical and mismatched repeats, implicating faulty replication as a causal mechanism for both pathways.

This work was supported by the National Institutes of Health (1 RO1 CA123203-01A1 to Drs. Paul Hasty and Cristina Montagna, 2P01AG017242-12 to Dr. Hasty, P30CA013330 to Dr. Montagna) and with support from the Cancer Therapy & Research Center at The University of Texas Health Science Center at San Antonio (P30 CA054174).

Two Replication Fork Maintenance Pathways Fuse Inverted Repeats to Rearrange Chromosomes. DOI: 10.1038/nature12500

For current news from the UT Health Science Center San Antonio, please visit our news release website, like us on Facebook or follow us on Twitter.

The Cancer Therapy & Research Center (CTRC) at The University of Texas Health Science Center at San Antonio is one of the elite academic cancer centers in the country to be named a National Cancer Institute (NCI) Designated Cancer Center, and is one of only four in Texas. A leader in developing new drugs to treat cancer, the CTRC Institute for Drug Development (IDD) conducts one of the largest oncology Phase I clinical drug programs in the world, and participates in development of cancer drugs approved by the U.S. Food & Drug Administration. For more information, visit http://www.ctrc.net.

Original press release: http://www.eurekalert.org/pub_releases/2013-09/uoth-ti2090513.php