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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.

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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 April 25, 2014

 

Cells in females (having two X chromosomes, identified as XX cells) are subtly but fundamentally
different from cells that are XY cells found in males. And, they remain different throughout all body
tissues and organs in each sex. This distinction may reflect the differences between male
and female response to medical treatment and severity of similar diseases.

Green — X chromosome   Blue — Y chromosome






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Y genes — some are essential to male survival

Despite a well-documented history of dramatic genetic decay, the human Y chromosome has over the course of millions of years of evolution managed to preserve a small set of genes that not only ensured their own survival but the survival of men. The vast majority of these tenacious genes appear to have little if any role in sex determination or sperm production.

Taken together, these remarkable findings—published in the journal Nature—suggest that because these Y-linked genes are active across the body, they may actually be contributing to differences in disease susceptibility and severity observed between men and women.

Whitehead Institute Director David Page conducted the research with collaborators from Washington University in St. Louis and Baylor College of Medicine.


"This paper tells us that not only is the Y chromosome here to stay, but that we need to take it seriously, and not just in the reproductive tract.

"There are approximately a dozen genes conserved on the Y that are expressed in cells and tissue types throughout the body. These are genes involved in decoding and interpreting the entirety of the genome. How pervasive their effects are is a question we throw open to the field, and it's one we can no longer ignore."

David Page, Director, Whitehead Institute for Biomedical Research, a Howard Hughes Medical Institute investigator and a professor of biology at Massachusetts Institute of Technology


Page believes this research will at last allow his lab to transition from proving the so-called rotting Y theorists wrong to a new era in Y chromosome biology. Over the past decade, Page and his group have been debunking the thinly supported but wildly popular argument that because the Y chromosome had lost hundreds of its genes over roughly 300 million years of evolution, its ultimate extinction is inevitable.


The loss of genetic content on the Y is not in dispute. In fact, a recent study from Page's own lab showed that the human Y chromosome retains only 19 of the more than 600 genes it once shared with its ancestral autosomal partner, the X chromosome.

However, by comparing the sequence of the human Y chromosome with that of the chimpanzee and the rhesus macaque, the lab discovered that the human Y has lost only one ancestral gene over the past 25 million years. Since then, the Y has been more than holding its own.


Having shown that the human, chimp, and rhesus Y chromosomes share nearly identical ancestral gene content, the lab set out in this latest work to map the evolution of the Y chromosomes of five more distantly-related mammals: the marmoset, mouse, rat, bull, and opossum. A comparison of the ancestral portions of these Y chromosomes revealed a set of broadly expressed genes across all eight species. Such genetic stability and conservation is no accident.

"This is not just a random sampling of the Y's ancestral repertoire," says Page, noting that each of the conserved genes discovered has a counterpart on the X chromosome. "This is an elite bunch of genes."

"Evolution is telling us these genes are really important for survival," adds Winston Bellott, a research scientist in the Page lab and lead author of the Nature paper. "They've been selected and purified over time."


Bellott and Page say the next phase of their research is to determine what this set of Y genes is actually doing, as they concede that's simply not yet clear.

What is clear, they argue, is that cells in females (which, having two X chromosomes, are referred to as XX cells) are subtly but fundamentally different from cells that are XY in males. And, they are different throughout the body in tissues and organs that show no obvious anatomic differentiation.


"They're similar but biologically different," says Bellott. "Yet, we have cell biologists and biochemists actively studying cells without any idea whether the cells are XX or XY. This is so fundamental to biology and biomedicine, and yet no one's really paid much attention to it."

Both Page and Bellott say what's needed is a biochemical catalog of the differences between XX and XY cells, including variability in such processes as gene expression and protein production. Page believes this pursuit could have enormous implications for human health.

"There is a clear need to move beyond a unisex model of biomedical research," Page says, "which means we need to move beyond a unisex model of our understanding and treatment of disease."

Abstract
The human X and Y chromosomes evolved from an ordinary pair of autosomes, but millions of years ago genetic decay ravaged the Y chromosome, and only three per cent of its ancestral genes survived. We reconstructed the evolution of the Y chromosome across eight mammals to identify biases in gene content and the selective pressures that preserved the surviving ancestral genes. Our findings indicate that survival was nonrandom, and in two cases, convergent across placental and marsupial mammals. We conclude that the gene content of the Y chromosome became specialized through selection to maintain the ancestral dosage of homologous X–Y gene pairs that function as broadly expressed regulators of transcription, translation and protein stability. We propose that beyond its roles in testis determination and spermatogenesis, the Y chromosome is essential for male viability, and has unappreciated roles in Turner’s syndrome and in phenotypic differences between the sexes in health and disease.


This work was supported by the National Institutes of Health and the Howard Hughes Medical Institute.

Written by Matt Fearer

David Page's primary affiliation is with Whitehead Institute for Biomedical Research, where his laboratory is located and all his research is conducted. He is also a Howard Hughes Medical Institute investigator and a professor of biology at Massachusetts Institute of Technology.

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