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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 Sep 3, 2013

 

All fetuses initially develop with female tissues, no matter
what the chld's sex will be at birth, so a master switch is responsible
for initiating the transformation of female tissues into male tissues.





WHO Child Growth Charts

 

 

 

Boy interrupted: Y-chromosome mutations reveal how precariousness is 'male'

The idea that men and women are fundamentally different from each other is widely accepted. And throughout the world, this has created distinct ideas about which social and physical characteristics are necessary in each gender to maintain healthy human development.

However, social revolutions throughout the last century have challenged traditional ideas about not only which traits are normal and necessary for survival, but also how humans acquire them. Thanks to a new study from researchers at Case Western Reserve University, science is continuing the charge.


By studying rare families in which a daughter shares a Y chromosome with her father, Michael Weiss, MD, PhD, and colleagues at Case Western University's School of Medicine, determined that the path to male sexuality is not as consistent or robust as scientists had always assumed.


A team led by Weiss, chairman of the Department of Biochemistry, the Cowan-Blum Professor of Cancer Research, and a professor of biochemistry and medicine, has published a study in the Proceedings of the National Academy of Sciences that examines the function of the SRY gene. This gene is responsible for initiating the process that leads to male development.

"A general principle of developmental biology is that evolution favors reliability," Weiss explained. "Robust switches ensure that our genetic programs give rise to a consistent body plan to ensure that babies have one heart, two arms, ten fingers, and so forth."

Traditional viewpoints emphasize the uniformity of this process. The new research indicates that male sexual development is less stable than other genetic programs.


In fetal development, a gene—called SRY—is located on the Y chromosome and begins the process leading to male development. All fetuses initially develop with female tissues, no matter what the sex will be at birth, so a master switch is responsible for initiating the transformation of female tissues into male tissues.

From there, the testes develop and produce testosterone, which eventually forms the male's external genitalia.


The university's study employs mutated SRY genes shared by a father and a sterile XY daughter. Females usually develop with an XX pair, but, in these families, the father instead produced a daughter with an XY pair. This occurs during fetal development when the SRY gene's master switch fails to trigger.

Internal female tissues, such as the uterus and fallopian tubes, continue to develop but are dysfunctional and infertile.

"Yet the father has the same Y chromosome and the same mutation as the daughter," Weiss pointed out. "And since he is a fertile male, we know that the switch must be poised right on its edge."

The team decided to measure the biochemical threshold of the SRY master switch.

Weiss: "Our expectation was that we'd find that a factor of 100 or more—a severe insult to the Y-encoded switch—was necessary to alter development. But what we found was that the SRY threshold, as probed in father-daughter pairs, is only a factor of two."

Therefore, human males actually develop near the edge of sexual ambiguity. This means that, unlike the robust genetic programs which develop other essential processes like heart function, the SRY gene master switch is particularly vulnerable to change. It only takes a slight deviation from the normal process to dramatically alter fetal sexual development.

Given the importance of sexual reproduction to the survival of a species, why do human SRY genes function so close to the boundary of infertility? The idea of an unreliable master switch might appear paradoxical, but a growing body of research suggests that it might be an evolutionary necessity.

Extensive studies of gender-associated styles of childhood play and the acquisition of social competencies by Dr. S. Baron-Cohen and colleagues at Cambridge University (UK) have highlighted the long-term effects of testosterone secretion by the fetal testis. Testosterone influences the patterning of the male brain during a critical window in human development.

And it is the SRY gene that sparks the genetic program leading to the formation of testes and the production of fetal testosterone.


"We have this tenuous switch on the Y chromosome, and we anticipate that its gift to humanity is variability in the pathway of male development from its earliest stages.

The essential idea is that our evolution has favored a broad range of social competencies. In prehistory, this range would have given a survival advantage to communities enriched by a diversity of gender styles."

Michael Weiss, chairman of the Department of Biochemistry, the Cowan-Blum Professor of Cancer Research, Case Western University


In fact, certain aspects of modern history seem to parallel this idea.

Susan Case, PhD, a professor of organizational behavior at Case Western Reserve Weatherhead School of Management, who was not involved in the study, agreed with Weiss's argument and noted that "diverse mixes of people offer more varied perspectives, more ideas and solutions, and more challenges to long-accepted views." In the corporate world, for example, these differing styles increase creativity and problem solving, especially within a group.

The implications of Weiss's research suggest that elements of human culture, which had been assumed to be psychological or cultural, may be biological, instead. Therefore, human evolution would not have been dependent on consistency and homogeneity, but on their exact opposite.

Significance
Gene duplication is prominent among evolutionary pathways through which novel transcription factors and gene regulatory networks evolve. A model in mammals is provided by Sry, a Y-encoded Sox factor that initiates male development. We provide evidence that a CAG DNA microsatellite invasion into the Sry gene of a rodent superfamily enabled its rapid evolution. This unstable microsatellite encodes a variable length glutamine-rich repeat domain. Our results suggest that intragenic complementation between the glutamine-rich domain and canonical Sry motifs accelerated their divergence through repeat length–dependent biochemical linkages. Such novelty may underlie emergence of non–Sry-dependent mechanisms of male sex determination.

Abstract
The male program of therian mammals is determined by Sry, a transcription factor encoded by the Y chromosome. Specific DNA binding is mediated by a high mobility group (HMG) box. Expression of Sry in the gonadal ridge activates a Sox9-dependent gene regulatory network leading to testis formation. A subset of Sry alleles in superfamily Muroidea (order Rodentia) is remarkable for insertion of an unstable DNA microsatellite, most commonly encoding (as in mice) a CAG repeat–associated glutamine-rich domain. We provide evidence, based on an embryonic pre-Sertoli cell line, that this domain functions at a threshold length as a genetic capacitor to facilitate accumulation of variation elsewhere in the protein, including the HMG box. The glutamine-rich domain compensates for otherwise deleterious substitutions in the box and absence of nonbox phosphorylation sites to ensure occupancy of DNA target sites. Such compensation enables activation of a male transcriptional program despite perturbations to the box. Whereas human SRY requires nucleocytoplasmic shuttling and coupled phosphorylation, mouse Sry contains a defective nuclear export signal analogous to a variant human SRY associated with inherited sex reversal. We propose that the rodent glutamine-rich domain has (i) fostered accumulation of cryptic intragenic variation and (ii) enabled unmasking of such variation due to DNA replicative slippage. This model highlights genomic contingency as a source of protein novelty at the edge of developmental ambiguity and may underlie emergence of non–Sry-dependent sex determination in the radiation of Muroidea.

nucleocytoplasmic trafficking protein–DNA recognition sexual dimorphism transcriptional activation triplet expansion

About Case Western Reserve University School of Medicine
Founded in 1843, Case Western Reserve University School of Medicine is the largest medical research institution in Ohio and is among the nation's top medical schools for research funding from the National Institutes of Health. The School of Medicine is recognized throughout the international medical community for outstanding achievements in teaching. The School's innovative and pioneering Western Reserve2 curriculum interweaves four themes--research and scholarship, clinical mastery, leadership, and civic professionalism--to prepare students for the practice of evidence-based medicine in the rapidly changing health care environment of the 21st century. Nine Nobel Laureates have been affiliated with the School of Medicine.

Annually, the School of Medicine trains more than 800 MD and MD/PhD students and ranks in the top 25 among U.S. research-oriented medical schools as designated by U.S. News & World Report's "Guide to Graduate Education."

The School of Medicine's primary affiliate is University Hospitals Case Medical Center and is additionally affiliated with MetroHealth Medical Center, the Louis Stokes Cleveland Department of Veterans Affairs Medical Center, and the Cleveland Clinic, with which it established the Cleveland Clinic Lerner College of Medicine of Case Western Reserve University in 2002. http://casemed.case.edu

Original press release: http://www.eurekalert.org/pub_releases/2013-09/cwru-biy082913.php