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Click weeks 0 - 40 and follow fetal growth
Defending the Genome
Multiple Sclerosis Not an Immune System Disease
Toddlers Rely On Others To Monitor Their Speech
How Pregnancy Changes a Woman’s Brain
New Device To Support Improved Newborn Health
Weight Reduction Through Mindful Eating
Breast Cancer, Heart Disease Share Common Roots
Breastfeeding Promotes Healthy Growth
First Months of Life Shape Flavor Preferences
Babies Remember Even As They Seem to Forget
Safer Treatment for Asthma, Allergies, Arthritis?
Endometriosis Link to Inflammatory Bowel Disease
Gene Discovered that Causes Rare Infant Epilepsy
Don't Buy Noisy Toys!
Childhood Cancer Drugs Cure, Later Cause Problems
Small, mobile sequences of DNA left over from viruses, called transposons or "jumping genes" (because of their ability to move around the genome), pose a significant threat to the genetic integrity and stability of any organism.
Considered genetic parasites, transposons are believed to make up as much as 50 percent of the human genome. Because of the damage they can do to DNA, an immune-like response has evolved to turn off, or silence, them.
New research published in the journal Cell by the labs of William E. Theurkauf and Zhiping Weng at the University of Massachusetts Medical School, sheds light on how the genome defends itself from these invading DNA parasites.
While it's known that specific small RNAs called Piwi-interacting RNAs (piRNAs) are responsible for turning off transposons, how isn't fully understood.
"The genome is littered with transposons," said William E. Theurkauf, PhD, professor of molecular medicine at UMass Medical School and lead author of the study. "In Drosophila there are over 120 different forms of transposons and these are the active pathogen that we are looking at in this host-pathogen response. Meanwhile, piRNAs are produced from regions of the genome that contain bits and pieces of transposons, and are the foundation for how these elements get silenced."
To understand how a genome responds to the introduction of a new transposon, Theurkauf and colleagues turned to a wild Drosophila, or fruit flies.
Unlike standard lab-bred fruit flies, wild Drosophila contain a transposon called the P element that first appeared after scientists started breeding fruit flies in the early part of the 20th century. Lab-bred fruit flies lack the P element transposon and the maternally inherited piRNA that can silence it.
When lab-bred females are crossed with P element-carrying wild fruit flies, the off-spring are unable to turn off the invading transposon and are sterile as a result.
However, Jaspreet Khurana, a PhD student in Theurkauf's lab observed that as these flies aged the hybrids regained fertility.
"Based on the observation that the flies recovered, it seemed likely that they were learning how to shut down transposons. We decided to use their system to look at the process of adaptation to a new transposable element," said Theurkauf.
Using a multi-disciplinary approach, Theurkauf and colleagues were able to get a complete genetic sequence of the sterile, hybrid flies at various stages of development.
What they found was startling.
In the hybrid off spring, the new transposon had triggered a response that disrupted the entire piRNA machinery. Not only was the newly introduced transposon jumping around the genome and causing a problem which was expected but most of the 120 plus transposons in the Drosophila genome had also become active.
"This massive destabilization of the genome is probably why they're sterile," said Theurkauf.
As the hybrids aged, however, the new transposon and all the existing, resident transposons, got shut down and fertility was restored.
"We found there were two mechanisms responsible for silencing the transposons," said Weng. "For P elements it turned out the flies learned to process the piRNA transcripts inherited from the father and turn them into mature piRNAs and silence the transposon."
"The bottom line on our study is when you introduce a single, new transposon it leads to a genetic crisis that activates all the transposons in the genome and compromises fertility in these hybrids," said Theurkauf.
"Remarkably, what emerges at the other end is an organism with an altered genome architecture that functionally recharges the piRNA clusters so they more effectively silence transposons."
The University of Massachusetts Medical School, one of the fastest growing academic health centers in the country, has built a reputation as a world-class research institution, consistently producing noteworthy advances in clinical and basic research. The Medical School attracts more than $307 million in research funding annually, 80 percent of which comes from federal funding sources. The mission of the Medical School is to advance the health and well-being of the people of the commonwealth and the world through pioneering education, research, public service and health care delivery with its clinical partner, UMass Memorial Health Care. For more information, visit www.umassmed.edu.
Original article: http://www.eurekalert.org/pub_releases/2011-12/uomm-dtg122111.php
|When grown-ups and kids speak, they listen to the sound of their voice and make corrections based on that auditory feedback. But new evidence shows that toddlers don't respond to their own voice in quite the same way, according to a report published online on December 22 in Current Biology, a Cell Press publication.|
|The findings suggest that very young children must have some other strategy to control their speech production, the researchers say.|
|"As they play music, violinists will listen to the notes they produce to ensure they are in tune," explained Ewen MacDonald of the Technical University of Denmark. "If they aren't, they will adjust the position of their fingers to bring the notes back in tune. When we speak, we do something very similar. We subconsciously listen to vowel and consonant sounds in our speech to ensure we are producing them correctly. If the acoustics of our speech are slightly different from what we intended, then, like the violinists, we will adjust the way we speak to correct for these slight errors. In our study, we found that four-year-olds monitor their own speech in the same way as adults. Surprisingly, two-year-olds do not."|
|That's despite the fact that infants readily detect small deviations in the pronunciation of familiar words and babble in a manner consistent with their native language. By the time they turn two, American children have an average vocabulary of about 300 words and appear well on their way to acquiring the sound structure of their native language.|
|In the experiment, adults, four-year-olds, and two-year-olds said the word "bed" repeatedly while simultaneously hearing themselves say the word "bad." (To elicit those utterances from the young children and toddlers, the researchers developed a video game in which players help a robot cross a virtual playground by saying the robot's 'magic' word "bed.")|
|"If they repeat this several times, adults spontaneously compensate, changing the way they say the vowel," MacDonald said. "Instead of saying the word 'bed,' they say something more like the word 'bid.'"|
|Four-year-olds adjusted their speech, too, the researchers show. The two-year-olds, on the other hand, kept right on saying "bed."|
|MacDonald says the results suggest a need to reconsider assumptions about how children make use of auditory feedback. It may be that two-year-olds depend on their parents or other people to monitor their speech instead of relying on their own voice. MacDonald notes that caregivers often do repeat or reflect back to young children what they've heard them say.|
|While this study involved children with normal speech development, MacDonald says they'll be exploring potential applications for understanding or addressing delayed and abnormal early speech development.|