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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 9, 2013

 


Mitochondria are microscopic reactors that burn oxygen to make ATP,
the basic unit of chemical energy in cells. As such, they are
the major consumers of the oxygen we breathe.







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Survival for stressed mitochondria discovered

Damage to mitochondria is thought to be a significant factor in common neurodegenerative disorders, cancer and even the aging process. Researchers' latest discovery could lead to new methods to protect mitochondria from such damage.

Scientists at The Scripps Research Institute (TSRI) have discovered a natural mechanism that cells use to protect mitochondria, the tiny but essential "power plants" that provide chemical energy for cells throughout the body.

"The mechanism that we've identified potentially gives us another way to treat the many disorders that involve mitochondrial dysfunction," said R. Luke Wiseman, the Arlene and Arnold Goldstein Assistant Professor in TSRI's Department of Molecular & Experimental Medicine.

Wiseman was the senior author of the new study, which appears in the December 3, 2013 issue of the journal Cell Metabolism.

Power Plants of the Cell

Mitochondria are microscopic reactors that burn oxygen to make ATP, the basic unit of chemical energy in cells. As such, they are the major consumers of the oxygen we breathe.


Oxygen molecules concentrated within mitochondria are highly reactive, tending to modify proteins in unwanted ways, changing them into abnormal shapes and often causing them to become dysfunctional and clump together.

If this misfolding and aggregation gets out of control—induced by factors including genetic mutations, aging and environmental toxins such as pesticides—the result can be the failure of mitochondria and cell death.


To help protect themselves from excess protein misfolding and aggregation, cells have evolved signaling pathways that protect mitochondria during stress.

These pathways primarily function by increasing the production of mitochondrial "chaperone" molecules that help keep proteins within mitochondria folded properly and protease enzymes that can cut up misfolded and aggregated mitochondrial proteins.

"These signaling pathways that regulate mitochondrial 'proteostasis' mechanisms, as we call them, have so far been poorly characterized in mammalian cells, but on the whole, they seem very important for cellular survival under stress," said Wiseman.

Reducing the Burden

In the new study, Wiseman and members of his laboratory, including first authors Kelly Rainbolt and Neli Atanassova focused on a third mechanism of mitochondrial proteostasis regulation: the reduced "import" of proteins into mitochondria.

"We predicted that reducing the population of newly imported proteins entering mitochondria would reduce the burden on mitochondrial chaperones and proteases during cell stress," said Rainbolt.

The team started by examining a protein complex, TIM23, which works as one of the chief importers of proteins into the inner section, or matrix, of mitochondria. TIM23 contains a core subunit called Tim17, which—uniquely in mammals—has two almost-identical variants, Tim17A and Tim17B, that incorporate into distinct complexes. The researchers used an environmental toxin, arsenite, to induce a general stress response in cultured mammalian cells and monitored alterations in Tim17A and Tim17B.

Results showed that Tim17A levels in the cells' mitochondria fell sharply in response to arsenite, while Tim17B levels were unaffected.

The authors found that the decrease in Tim17A was induced downstream of an established biologic signaling pathway that protects cells during stress.

The decrease in Tim17A occurred not only because Tim17A production was reduced, but also because Tim17A was degraded more rapidly than usual.

The team soon found that a mitochondrial protease, YME1L, is responsible for the stress-induced degradation of Tim17A.

"The capacity for an established, protective biologic signaling pathway to induce Tim17A degradation indicated to us that Tim17A degradation is likely a protective mechanism to promote mitochondrial proteostasis in response to pathologic insults," said Rainbolt.


In fact, the scientists showed that reducing Tim17A protein levels increased cellular survival in response to stresses that directly challenge mitochondrial proteostasis and function.

Alterations in mitochondrial proteostasis mechanisms are common to many human diseases, including cancer and neurodegenerative disorders such as Alzheimer's disease and Parkinson's disease.


Wiseman notes that the identification of new cellular mechanisms regulating mitochondrial proteostasis, such as Tim17A degradation, suggests potential new therapy approaches to corrrect mitochondrial dysfunction in related diseases.

Abstract
Highlights
Tim17A is a stress-sensitive subunit of the TIM23 protein import complex
Tim17A protein decreases in response to stress-regulated translation attenuation
Tim17A degradation requires the activity of the mitochondrial protease YME1L
Decreased Tim17A/Tim-17 is protective against oxidative stress

Summary
Stress-regulated signaling pathways protect mitochondrial proteostasis and function from pathologic insults. Despite the importance of stress-regulated signaling pathways in mitochondrial proteome maintenance, the molecular mechanisms by which these pathways maintain mitochondrial proteostasis remain largely unknown. We identify Tim17A as a stress-regulated subunit of the translocase of the inner membrane 23 (TIM23) mitochondrial protein import complex. We show that Tim17A protein levels are decreased downstream of stress-regulated translational attenuation induced by eukaryotic initiation factor 2α (eIF2α) phosphorylation through a mechanism dependent on the mitochondrial protease YME1L. Furthermore, we demonstrate that decreasing Tim17A attenuates TIM23-dependent protein import, promotes the induction of mitochondrial unfolded protein response (UPR)-associated proteostasis genes, and confers stress resistance in C. elegans and mammalian cells. Thus, our results indicate that Tim17A degradation is a stress-responsive mechanism by which cells adapt mitochondrial protein import efficiency and promote mitochondrial proteostasis in response to the numerous pathologic insults that induce stress-regulated translation attenuation.


Authors
T. Kelly Rainbolt, Neli Atanassova, Joseph C. Genereux, R. Luke Wisemansend

The study, "Stress-Regulated Translational Attenuation Adapts Mitochondrial Protein Import Through Tim17A Degradation," was also co-authored by Joseph C. Genereux of Wiseman laboratory at TSRI.

Funding for the research was provided by the Ellison Medical Foundation, Arlene and Arnold Goldstein and the National Institutes of Health (R01 AG036634).