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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 18, 2013

 

In this image, (left) the endoplasmic reticulum (ER) of a cell with the Mfn2 protein and (right) without it.
On the right, the ER formed vesicles indicate that the organelle is completely disorganized and unable to respond correctly to cellular stress.

Image crdit: JP Muñoz






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A protein that can mean life or death for a cell

Researchers have discovered that Mitofusin 2 confers the cell with the sensitivity to understand its own state of health, determine whether it should be repaired or even undergo apoptosis (cell death).


With this new function, Mitofusin 2 becomes a viable target to intervene in diseases such as neurodegeneration and cancer.

Each cell in an organism has a sensor that measures the health of its "internal" environment.

This "alarm" is found in the endoplasmic reticulum (ER), which is able to sense cellular stress and trigger either rescue responses or the death of the cell.


A team from the Institute for Research in Biomedicine (IRB), in Barcelona, has discovered that the protein Mitofusin 2 (Mfn2) plays a crucial role in correctly measuring stress levels, and also makes sure the pathways of cell repair or cell death are effective.

The research revealed some of the molecular mechanisms that connect Mfn2 to endoplasmic reticulum stress, in the latest edition of the EMBO Journal, from the Nature Group, published by the European Molecular Biology Organization.

When the scientists removed Mfn2 from the cell under conditions of cell stress, the endoplasmic reticulum responded by over-activating the repair pathways. By doing so, it contradictorily functioned worse, reducing the capacity of cells to overcome the stress insult and promoting to a lesser degree apoptotic cell death. “When Mfn2 is removed, the cellular stress response pathways are completely disrupted,” says Antonio Zorzano, coordinator of IRB’s Molecular Medicine Programme and leader of the group “Heterogenic and polygenic diseases."

Not only diabetes

Mfn2 is a mitochondrial protein whose deficiency is related to diabetes. In an earlier publication in Proceedings of the National Academy of Sciences (PNAS), Dr. Zorzano’s research team demonstrated that without Mfn2, tissues become resistant to insulin, a characteristic of diabetes and the so-called metabolic syndrome. In this study, they also observed that the cells had higher endoplasmic reticulum stress.


The current study investigates the relationship between mitochondria and the endoplasmic reticulum, and indicates that changes in mitochondria, caused by the loss of the Mfn2 protein, directly affects endoplasmic reticulum function.


“We have shown that Mfn2 is important for cell viability and has implications for numerous diseases, such as neurodegeration, cancer, cardiovascular disease, in addition to diabetes,” says postdoctoral researcher Juan Pablo Muñoz, first author of the study.


Is Mitofusin 2 a good therapeutic target?


“The fact that we can modulate cell damage response with Mfn2 opens a wide window of possible therapeutic avenues for further study,” says Muñoz. The Chilean scientist at IRB explains that tumour cells don’t activate cell death properly and proliferate uncontrolled. “Cancer cells have already been noted to have low Mfn2 levels, and if we could increase such levels, we would be able to promote apoptosis,” he continues. According to this, other research teams have already published work indicating that the overexpression of Mfn2 induce apoptosis.

To demonstrate the utility of Mfn2 as a target, the researchers now need to find a small molecule, or drug, that modulates its expression in animals. “Our work published on Mfn2 is a proof of concept that highlights the importance of this mitochondrial protein for cell health,” says Zorzano. One of the challenges of the group is to secure funding to perform a massive screening of molecules with the ability to modulate Mfn2 expression and confirm its effects in mice.

Abstract
Mitofusin 2 (Mfn2) is a key protein in mitochondrial fusion and it participates in the bridging of mitochondria to the endoplasmic reticulum (ER). Recent data indicate that Mfn2 ablation leads to ER stress. Here we report on the mechanisms by which Mfn2 modulates cellular responses to ER stress. Induction of ER stress in Mfn2-deficient cells caused massive ER expansion and excessive activation of all three Unfolded Protein Response (UPR) branches (PERK, XBP-1, and ATF6). In spite of an enhanced UPR, these cells showed reduced activation of apoptosis and autophagy during ER stress. Silencing of PERK increased the apoptosis of Mfn2-ablated cells in response to ER stress. XBP-1 loss-of-function ameliorated autophagic activity of these cells upon ER stress. Mfn2 physically interacts with PERK, and Mfn2-ablated cells showed sustained activation of this protein kinase under basal conditions. Unexpectedly, PERK silencing in these cells reduced ROS production, normalized mitochondrial calcium, and improved mitochondrial morphology. In summary, our data indicate that Mfn2 is an upstream modulator of PERK. Furthermore, Mfn2 loss-of-function reveals that PERK is a key regulator of mitochondrial morphology and function.

Reference article:
Mfn2 modulates the UPR and mitochondrial function via repression of PERK
Juan Pablo Muñoz, Saška Ivanova, Jana Sánchez-Wandelmer, Paula Martínez-Cristóbal, Eduard Noguera, Ana Sancho, Angels Díaz-Ramos, María Isabel Hernández-Alvarez, David Sebastián, Caroline Mauvezin, Manuel Palacín and Antonio Zorzano
The EMBO Journal (2013) 32, 2348 - 2361. doi:10.1038/emboj.2013.168

Original press releas: http://www.irbbarcelona.org/index.php/en/news/irb-news/scientific/a-protein-that-can-mean-life-or-death-for-cells