The parasite Toxoplasma gondii (red) causes mitochondria (green) to shed large structures of their "skin" (yellow).
© Xianhe Li/Max Planck Institute for Biology of Ageing, 2022
Creationist mode: 
Here is yet another example of the evil genius that Creationists believe created everything, including parasites that, if they were designed at all, could only have been designed for the sole purpose of making humans and other animals and plants sick and die.
One of the problems the allegedly intelligent designer had to design a solution to was the mechanisms it had designed earlier for protecting us from these nasty little products of its sadistic mind. In this paper, researchers led by Lena Pernas of the Max Planck Institute for Biology of Ageing in Cologne, Germany, have shown how parasitic pathogens can turn off mitochondrial defence mechanisms by hijacking a normal cellular response to stress.
As the Max Planck Institute for Biology of Aging, news release explains:
To survive, pathogens need to acquire nutrients from their host and counter host defenses. One such defense comes from host mitochondria, which can deprive them of nutrients they need and thus restrict their growth. “We wanted to know how else mitochondrial behaviour changes when mitochondria and pathogens meet in cells. Because the outer membrane of these organelles is the first point of contact with the pathogens, we took a closer look at it,” explains Lena Pernas, research group leader at the Max Planck Institute for Biology of Ageing.
In [binding to a receptor on the outer membrane of mitochondria], the parasite hijacks a normal host response to mitochondrial stress that, in the context of infection, effectively disarms the mitochondria. Other researchers have shown that a SARS-CoV-2 virus protein also binds to this transport receptor. This suggests the receptor plays an important role in the host-pathogen interaction. But further investigation is needed to better understand its role during different infections.Mitochondria shed their ´skin`
Lena F Pernas, team leader
Max Planck Institute for Biology of Ageing
Cologne, Germany.
The researchers infected cells with the human parasite Toxoplasma gondii and observed live under the microscope what happens to the outer compartment of mitochondria. "We saw that mitochondria in contact with the parasite started shedding large structures from their outer membrane. This was so puzzling to us. Why would mitochondria shed what is essentially the gateway between them and the rest of the cell?" says Xianhe Li, first author of the study.
Hostile takeover
But how does the parasite get the mitochondria to do it? The research team was able to show that the pathogen has a protein that functionally mimics a host mitochondrial protein. It binds to a receptor on the outer membrane of mitochondria, to gain access to the machinery that ensures proteins are transported inside the mitochondria.
Creationist mode: 
The team explain more in the structured abstract to their paper published in Science yesterday:
Structured AbstractOnce again then, if you believe in the childish notion of intelligent design, you have another example of the lengths your beloved sadist has gone to make us sick. And of course, being a follower of one of the flavours of the Abrahamic religions, you are obliged by dogma to believe that there is only one entity capable of creating these parasites and that any resulting arms races and designs intended to overcome the defences it designed earlier are with and against itself.
INTRODUCTION
Mitochondria are dynamic organelles that coordinate many cellular functions that are essential for life, including diverse metabolic processes, cell division and differentiation, and immune signaling. To carry out these diverse functions, mitochondria must communicate with the cytosol, a task mediated by the outer mitochondrial membrane (OMM), the gateway between mitochondria and the rest of the cell. Thus, preserving the integrity of the OMM is essential for cellular homeostasis. Although responses to stress that is artificially induced by small molecules have been described, little is known of the mechanisms by which mammalian cells respond to naturally occurring stresses of the OMM.
RATIONALE
Several intracellular microbes come in contact with the host OMM or release proteins that target the OMM. We reasoned that microbial infection would serve as a model with which to study cellular responses to natural OMM stress. To this end, we chose the human parasite Toxoplasma gondii because it tethers host mitochondria to its parasite vacuole; in an infected cell, areas of close membrane apposition form between the host OMM and the parasite vacuole membrane. To address how Toxoplasma affected the OMM, we performed live-cell imaging of infected mammalian cells stably expressing OMM-targeted green fluorescent protein (GFP). We found that mitochondria in contact with the Toxoplasma vacuole released large structures that were positive for OMM, which we termed “SPOTs.” Analysis of SPOTs in fixed and live cells revealed that SPOTs did not contain proteins of the mitochondrial matrix and inner mitochondrial membrane (IMM).
RESULTS
Having identified Toxoplasma infection as a natural stress that induced OMM remodeling and the shedding of SPOTs, we next dissected how these structures are formed. We found that the secreted effector protein TgMAF1 (Toxoplasma gondii mitochondrial association factor 1), which tethers the host OMM to the parasite vacuole membrane, was required for SPOT formation. TgMAF1 led to a decrease in the amount of mitochondrial proteins during infection. In particular, the OMM proteins mitofusin 1 and mitofusin 2 were degraded during infection. These proteins, which mediate a nutritional defense against Toxoplasma by promoting mitochondrial uptake of fatty acids, localized to SPOTs. The ability of TgMAF1 to induce SPOTs depended on its binding to the host OMM import receptor TOM70 (translocase of the outer membrane 70), whose import function TgMAF1 impaired. TOM70 was required for optimal parasite growth and enabled an interaction between TgMAF1 and the OMM translocase SAM50 (sorting assembly machinery 50 kDa subunit), which is a key component of the OMM-IMM mitochondrial intermembrane space bridging (MIB) complex. The genetic ablation of SAM50 and the overexpression of an OMM-targeted protein induced the formation of SPOT-like structures independently of infection.
CONCLUSION
Because SAM50 is the only component of mitochondrial import machinery that bridges the OMM and IMM, it is in a position to translate OMM stress into the removal of compromised OMM. TgMAF1 behaves as a mitochondrial preprotein that uses the host receptor TOM70 to interact with SAM50. This enables Toxoplasma to hijack a cellular response to OMM stress—the formation of SPOTs—and drive the constitutive shedding of the OMM. Consequently, levels of mitochondrial proteins that restrict parasite growth are depleted, and import machinery that is required for mitochondrial biogenesis is sequestered on SPOTs. In an infection-independent context, however, we propose that SPOT-like structures could mitigate OMM stress by enabling the excision of dysfunctional OMM machinery, such as import receptors or translocases during defective import. Our finding that OMM remodeling occurs during infection and infection-independent scenarios sheds light on potential cellular mechanisms that safeguard OMM function.
Not only malevolent but stupid.
And that is the view you would prefer people to have of the god you purport to worship and whose religion you purport to promote. With friends like Creationists, what god needs enemies?
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