Protein 53 (or tumor protein 53), is a tumor suppressor protein that in humans is encoded by the TP53 gene. Since 2003, biophysicists have referenced this protein 53 (p53) to be a rheostat, or dimmer switch in laymen terms. Although this terminology is only meant to be a metaphor, there is much validity to the fact that p53 functions exactly as a dimmer switch. Ongoing examination of p53 indicates that it does more than operate as an on/off switch, but regulates ranges of values that are fine-tuned as needed in the cell.
Molecular Rheostats Control Expression of Genes
In 2003, a review paper published in the January 10 edition of Cell, entitled “Regulating the Regulators: Lysine Modifications Make Their Mark,” stated in the abstract:
Although the composition of this machinery is largely known, mechanisms regulating its activity by covalent modification are just coming into focus. Here, we review several cases of ubiquitination, sumoylation, and acetylation that link specific covalent modification of the transcriptional apparatus to their regulatory function. We propose that potential cascades of modifications serve as molecular rheostats that fine-tune the control of transcription in diverse organisms [The emphasis is mine].
In their 2003 review paper, Richard Freiman of Howard Hughes Medical Institute and Robert Tijian of UC Berkeley itemize numerous examples of how molecular systems regulate genes. The paper employs vocabulary terms such as “elaborate,” “intricate,” “exquisite,” and “dramatic.”
The paper begins by asserting the following:
The temporal and spatial control of gene expression is one of the most fundamental processes in biology, and we now realize that it encompasses many layers of complexity and intricate mechanisms. To begin understanding this process, researchers have identified and partly characterized the elaborate molecular apparatus responsible for executing the control of gene expression [emphasis mine].
The paper further describes molecular rheostat function, “The molecular machinery responsible for controlling transcription by RNA polymerase II (RNA pol II) is considerably more complex than anyone had anticipated.” [Emphasis added]. The Freiman and Tjian (2003) paper continues:
“It is not hard to envision that these lysine residues therefore serve as critical molecular switches that can respond to different signals in highly specific ways. In addition, since most proteins contain many lysine residues, transcription factors may undergo multiple modifications simultaneously or in sequential order, pointing to the possibility of generating complex networks of regulatory events.” [Emphasis mine]
Therefore, the Freiman and Tjian (2003) paper concludes:
“Clearly, transcription is exquisitely regulated in all organisms, and one mechanism utilized to achieve such regulation is covalent modification of the transcriptional machinery. Future studies in diverse organisms and specialized regulatory pathways should further illuminate how transcription factor modification contributes to the elaborate mechanisms of gene regulation.”
Molecular Rheostats In Tadpole Spinal Cord Development
A fresh new research paper just hot off the press is Zhang, Issberner and Sullar, “Development of a spinal locomotor rheostat,” PNAS June 27, 2011, published online before print June 27, 2011, doi: 10.1073/pnas.1018512108. In Zhang et al (2011), Scottish scientists examining Xenopus tadpole spinal cord development found that the first pools of neurons are all alike. The neurons rapidly sort out into ventral and dorsal domains within a day. During tadpole development, the neurons become more specialized as the tadpole requires increased need to swim with greater finesse.
The Zhang et al (2011) PNAS paper reads:
“This unfolding developmental plan, which occurs in the absence of movement, probably equips the organism with the neuronal substrate to bend, pitch, roll, and accelerate during swimming in ways that will be important for survival during the period of free-swimming larval life that ensues.” [Emphasis mine]
It is very difficult to avoid inferring from this quote that tadpole development features foresight as to what the tadpole will need, and fine-tunes the “rheostat” of neural specialization to permit the tadpole to interact with its environment.
Molecular Rheostats In Humans
Medical Express just recently reported that scientists at the Salk Institute for Biological Studies have found clues to the functioning of an important damage response protein in cells. The protein, p53, can cause cells to stop dividing or even to commit suicide when they show signs of DNA damage. Protein 53 is responsible for much of the tissue destruction that follows exposure to ionizing radiation or DNA-damaging drugs such as the ones commonly used for cancer therapy.
Geoffrey M. Wahl, professor in the Salk Institute’s Gene Expression Laboratory, describes p53 is “… like a dimmer switch, or rheostat, that helps control the level of p53 activity in a critical stem cell population and the offspring they generate.” Professor Wahl is the senior author of the study, which appears online in the journal Genes & Development on July 1, 2011. “In principle, controlling this switch with drugs could reduce the unwanted effects from DNA-damaging chemotherapy or radiation treatment, allowing higher doses to be used.”
The regulator protein p53 is a decision maker concern DNA repairs. Protein 53 decides whether repairs should proceed. If not, p53 commands the affected cell to commit suicide. Now, how’s that for intelligent design! The Salk Institute findings show “that a short segment on p53 is needed to fine-tune the protein’s activity in blood-forming stem cells and their progeny after they incur DNA damage [emphasis mine].”
The article notes that short segment is “an evolutionarily conserved regulatory segment of p53.” The term “conserved” is the word biologists use to reference a process that started out fully functioning and perfectly developed in its advanced state initially at the beginning of life, and since then has never evolved.
The Medical Express article goes on to say this about protein 53:
“One problem with p53 is that it apparently evolved to protect the integrity of the genome for future generations, rather than to prolong the lives of individual cells or animals. From the point of view of an animal, p53 sometimes goes too far in killing cells or suppressing growth.” [Emphasis mine].
Excuse me? Did the medical science journalist just say “evolve to”? Someone needs to remind Darwinists every once in a while that evolution does not evolve “to” do anything. Natural processes are supposed to be entirely unguided, and to suggest there is foresight implies teleology. Darwinists continue to remind each other that they need to quit using teleonomic language, but I suppose it is difficult mental gymnastics at times to avoid invoking intelligent design.
The existence of molecular rheostats and dimmer switches that fine-tune processes says nothing about how they came into existence and became fine-tuned. The only rheostats and dimmer switches we know about, even if they are broken ones, are intelligently designed.