More Bad News for Creationists - Their Putative Designer Designed Death and Suffering, Allegedly.

Buck Scientist Uncovers Clues to Aging in Mitochondria
For the want of a better answer, Bible-literalist creationist will tell you that before Adam and Eve and 'The Fall' there was no death in the world and that death is the result of 'sin', not designed by their god at all, so their god can't be held responsible for all the lethal organisms that cause so much ill health, death and suffering in the world. They never manage to explain where the food Adam and Eve ate was alive during the whole of the eating, digestion and metabolism of it though, or whether their god made an exception in that case and allowed a little bit of death, just not human death.

Now, however, they have some more mental gymnastics to perform with the discovery that it is the mitochondria in all our cells that are responsible for aging - a process that leads ultimately to death unless illness of some sort intervenes. Scientists have known about this for some time, but a team of scientists from the Buck Institute for Research on Aging have worked out how it happens. Mitochondria, the powerhouses inside every eukaryote cell, are believed to be the descendants of a bacteria related to rickettsia which became incorporated with other organelles inside prokaryote cells.

The mitochondria in our cell still have their own DNA and replicate inside our cells, although much of their original genome has been incorporated into the cell nucleus. Because only the head of the sperm penetrates the egg at fertilisation and the head contains no mitochondria, we get all our mitochondria and so all our mitochondrial DNA from our mother and none from our father.

Basically, aging is caused by imperfect mitochondrial replication which is accumulated over the years until the mitochondria start to malfunction. Because they have given up some of the DNA into the cell nucleus, they need to reactivate some of it and import the products of it before they can replicate themselves, and this is where the process begins to go wrong, according to the Buck team.

The Buck News release explains what the team led by Buck Fellow Chuankai (Kai) Zhou, PhD, has discovered:

Now that we have this different hypothesis of why mitochondrial dysfunction happens during aging and age-related diseases, we open a completely different way to think about, measure, mitigate and reverse that process.

Our research finding that the molecule Tom70 is coordinating both aspects bridges two separate fields of study.

We discovered a new function for this protein and we provide a mechanism of how Tom70 can do good things to the cell. Additionally, if our hypothesis proves to be true, it will naturally lead to products, such as supplements or drugs. It just takes time.

Chuankai (Kai) Zhou, PhD, senior author
Buck Institute for Research on Aging
Novato, USA
And USC Leonard Davis School of Gerontology
University of Southern California, Los Angeles, CA, USA

Mitochondria are commonly referred to as the “powerhouse” of the cell, as the bean-shaped structures provide the units of energy that every cell needs to function. They are involved in many critical processes, including immune response, inflammation, and metabolism.

Dysfunction of the mitochondria is implicated in most chronic diseases, said Zhou, including neurodegenerative disorders, cardiovascular diseases, cancer, diabetes, and obesity. A growing body of evidence indicates that this dysfunction contributes to aging in general.

Zhou’s team wanted to explore the contributions of “mitochondrial biogenesis” to the dysfunction of mitochondria during aging. Mitochondrial biogenesis is the cellular process that produces new mitochondria. It determines both the quality and quantity of mitochondria in cells, both of which decline during normal aging. In the past couple decades, scientists already described two major steps of mitochondrial biogenesis: the transcriptional activation of mitochondrial protein in the cellular nucleus in response to nutrient/metabolic signals and the import of these newly synthesized mitochondrial proteins from cytosol into mitochondria. However, it was unclear how these two steps of mitochondrial biogenesis coordinate with each other to streamline the synthesis and import of mitochondria proteins. Zhou’s team found that a conserved receptor molecule on the surface of mitochondria called Tom70 might be responsible for coordinating these two steps by regulating the transcriptional activity of mitochondrial proteins inside nucleus.

Tom70 is previously known to facilitate the import of newly synthesized mitochondrial proteins. However, Zhou noted, the amount of protein created must be fine-tuned to meet the needs and import capacity of the mitochondria but not overshoot production such that excess accumulates within the cell, which damages cells and can kill them.

In the current study, his team used yeast as the model to test whether Tom70 regulates mitochondrial biogenesis by coordinating the intricate balance between the production of proteins destined for the mitochondria and the rate that these proteins can be escorted into the mitochondria. They found that it did. Similar regulatory function of Tom70 is conserved in fruit flies.

The two processes of communication about needs and uptake into the mitochondria had not been previously linked.

Interestingly, they found that Tom70 declines during aging, which is associated with reduced mitochondrial biogenesis. Similar reductions of Tom70 were observed previously in aged fruit flies and rats. The team went on to show that increasing the level of Tom70 in yeast delayed mitochondrial dysfunction and increased lifespan. This finding ties in with what was known for more than a decade, that increasing Tom70 can protect human cells against some chronic diseases, such as cardiovascular disease, but the mechanistic details were not known about why this occurred.

Copyright: © 2022 The authors.
Published by eLife Sciences Publications Ltd. Open access. (CC BY 4.0)

The team's findings are published, open access, in the online journal eLife, which unusually also includes the editor's evaluation of the research:

Abstract

Mitochondrial biogenesis has two major steps: the transcriptional activation of nuclear genome-encoded mitochondrial proteins and the import of nascent mitochondrial proteins that are synthesized in the cytosol. These nascent mitochondrial proteins are aggregation-prone and can cause cytosolic proteostasis stress. The transcription factor-dependent transcriptional regulations and the TOM-TIM complex-dependent import of nascent mitochondrial proteins have been extensively studied. Yet, little is known regarding how these two steps of mitochondrial biogenesis coordinate with each other to avoid the cytosolic accumulation of these aggregation-prone nascent mitochondrial proteins. Here, we show that in budding yeast, Tom70, a conserved receptor of the TOM complex, moonlights to regulate the transcriptional activity of mitochondrial proteins. Tom70’s transcription regulatory role is conserved in Drosophila. The dual roles of Tom70 in both transcription/biogenesis and import of mitochondrial proteins allow the cells to accomplish mitochondrial biogenesis without compromising cytosolic proteostasis. The age-related reduction of Tom70, caused by reduced biogenesis and increased degradation of Tom70, is associated with the loss of mitochondrial membrane potential, mtDNA, and mitochondrial proteins. While loss of Tom70 accelerates aging and age-related mitochondrial defects, overexpressing TOM70 delays these mitochondrial dysfunctions and extends the replicative lifespan. Our results reveal unexpected roles of Tom70 in mitochondrial biogenesis and aging.

Editor's evaluation

The authors test the hypothesis that components of the TOM complex regulate efficient mitochondrial biogenesis by coordinating the synthesis (via controlling transcription of the corresponding RNAs) of mitochondrial proteins with the rate of mitochondrial protein import. It has previously been established that failure to import mitochondrial proteins results in the accumulation of toxic protein aggregates in the cytosol. The authors conclude that Tom70 fulfills this role and find that Tom70 expression declines as cells age, which contributes to age-associated mitochondrial dysfunction.

Qingqing Liu, Catherine E Chang, Alexandra C Wooldredge, Benjamin Fong, Brian K Kennedy, Chuankai Zhou (2022)
Tom70-based transcriptional regulation of mitochondrial biogenesis and aging
eLife 11:e75658 DOI: 10.7554/eLife.75658

Copyright: © 2022 The authors.
Published by eLife Sciences Publications Ltd. Open access
Reprinted under a Creative Commons Attribution 4.0 International license (CC BY 4.0)

So, why is this a problem for creationists?

Given that intelligent [sic] design advocates argue that a system as complex as mitochondria could not have arisen by evolution but must have been intelligently designed, they also have to accept that the mechanism by which they replicate, together with the problem of cell aging this leads to, as this study shows, must have been designed by their putative designer. In other words, they have to accept that death was either designed by their god and is not the consequence of something over which their supposedly omnipotent designer had no control, and was all the fault of a mythical ancestral couple, or that their god didn't understand what its creation would lead to, and couldn't correct its mistake once it saw what it had blundered into - just like a mindless, unintelligent, uncaring design process, in fact.

And of course, there is the common problem for ID advocates to explain - the massive complexity needed to achieve something that should have been simple to achieve for an omnipotent, intelligent designer, as we see so often when we look beneath the superficial in nature.

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Thank you for sharing!

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