July 11, 2023 | David F. Coppedge

Repair Implies Foresight Implies Design

Multiple mechanisms are at work maintaining
the body and repairing injuries to cells and tissues

 

A repair algorithm that restores function to a system of multiple operating parts implies at least three requirements: (1) the foresight to know which problems can occur, and (2) the ability to sense a problem, and (3) know-how to restore the system to full operation—or at least to prevent catastrophic failure. Could such capabilities evolve by chance?

Georgia State researchers use ORNL supercomputer to gain new insights into DNA repair (Oak Ridge National Lab, 7 July 2023). Consider what is required to get a repair system to change its own configuration for handling different tasks. Does this not presuppose intelligent design?

Transcription factor IIH, or TFIIH, pronounced “TF two H,” is a veritable workhorse among the protein complexes that control human cell activity. It plays critical roles both in transcription — the highly regulated enzymatic synthesis of RNA from a DNA template — and in the repair of damaged DNA. But how can one protein assembly participate in two such vastly different and extremely important genomic tasks?

A team of researchers led by chemistry professor Ivaylo Ivanov of Georgia State University used the Summit supercomputer at the Department of Energy’s Oak Ridge National Laboratory to help answer that question. By conducting multiple molecular dynamics simulations of TFIIH in transcription and DNA repair-competent states and then contrasting the structural mechanisms at work, Ivanov and his team made an interesting discovery: TFIIH is a shapeshifter, reconfiguring itself to meet the demands of each task.

UVA Discovers Repair Process That Fixes Damaged Hearing Cells (University of Virginia, 6 July 2023). Researchers at UVA Health System comment that “Hair cells are naturally fragile – they must be delicate so they can sense sound, but they also must withstand the continuous mechanical stress inherent in their jobs.” Yet these delicate hair cells, so easily damaged, can be restored at least partially by a naturally occurring repair process that first detects damage and then moves in to fix it.

Prolonged exposure to loud noise harms hair cells in a variety of ways, and one of those is by damaging the cores of the “hairs” themselves. These hair-like structures are known as stereocilia, and Shin’s new research shows a process they use to repair themselves.

The hair cells do this by deploying a protein called XIRP2, which has the ability to sense damage to the cores, which are made of a substance called actin. Shin and his team found that XIRP2 first senses damage, then migrates to the damage site and repairs the cores by filling in new actin.

The NIH granted Shin’s lab $2.3 million in funds for this research. Age-related hearing loss and other forms of deafness might find solutions by understanding and “harnessing internal mechanisms by which hair cells counteract wear and tear” in our inner ears.

The Human Cell showing some of its basic parts (Wiki commons)

Wound repair: Two distinct Rap1 pathways close the gap (Current Biology, 10 July 2023). The summary of this repair pathway brings up the design-based topics of coordination, repair, remodeling, and requirements.

Groups of cells often coordinate their movements during normal development, cancer invasion, and wound repair. These coordinated migrations require dynamic cytoskeleton and cell-junction remodeling. Two distinct Rap1 pathways are required to regulate this dynamic remodeling for rapid wound closure.

When cells need to move, the authors say, “Dynamic remodeling of the cytoskeleton and cell–cell junctions is indispensable to maintain connections between particular cells while moving with controlled direction and speed within the body.” This implies that signals must get into the cells of tissues and coordinate their actions while the repair cells get into position. They identified two enzymes that perform this coordination.

Rap1, a member of the Ras family of small GTPases, is a highly conserved [i.e., unevolved] cytoplasmic protein that regulates signal transduction pathways needed for the dynamic remodeling of the cytoskeleton and cell–cell adhesion. Rap1 is needed for a wide range of developmental events, including neural migration, leukocyte trafficking, promotion of angiogenesis, embryonic morphogenesis, and maintenance of the endothelial barrier, as well as being involved in pathological conditions, such as cancer metastasis and wound healing….

Using Drosophila embryonic epithelial wound repair as a model, a new study by Rothenberg and colleagues in this issue of Current Biology shows that two distinct Rap1 pathways are required to regulate the remodeling of cell–cell junctions and the cytoskeleton in order to drive rapid wound closure (Figure 2).

The details of just this repair system alone are stunning. (Here’s more detail in a related preprint today on bioRxiv about the migration of T cells in immune response.)

Yet there are many other repair systems in the body just as complicated, if not more so. How do these enzymes and cells know what to do, coordinating their actions, unless they had been programmed by a vast intelligence with the foresight to know they would be needed?

Darwinism dies in the details. These sources confirm our long-standing observation: the more detail is provided about living systems, the less talk about evolution. None of these articles or papers even mentioned it.

Damaged DNA-Repair Response Map. Diagram from Kratz, et al. A multi-scale map of protein assemblies in the DNA damage response. Cell Systems, 2023.

 

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