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Not Too Tart, Not Too Sweet: Fine-Tuned Gene Expression of Lamin Provides Evidence for Design

By Fazale Rana - April 1, 2009
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I live in a city in Southern California historically known for its lemon groves. Each spring the community celebrates its history with The Lemon Festival. Along with the weekend’s events, there is no shortage of great-tasting lemonade.

Even though the recipe is simple, exceptional lemonade requires careful attention to detail: the just-right amount of sugar must be added to the just-right amount of freshly squeezed lemon juice.

Biochemical systems are like good lemonade. The levels of their molecular components have to be carefully adjusted. And, as new research on lamin B1 attests, this precision is critical.1 If the amount of this key protein—found in the membrane surrounding a cell’s nucleus––is altered ever so slightly it leads to neurodegenerative disorders (for example, Alzheimer’s and multiple sclerosis).

Lamins play an important role in maintaining the structural integrity of the membrane that surrounds the nucleus. These proteins also serve as anchor points for the chromosomes found in the nucleus. (Chromosomes harbor the genetic information that the cell’s machinery needs to make proteins, the complex molecules that carry out the various processes in the cell.) Through their interaction with chromosomes, lamins control the production of proteins by regulating how the cell’s machinery accesses the information stored in the chromosomes.

Research indicates that specific neurodegenerative disorders result when lamin B1 is overproduced. This overproduction retards the maturation of oligodendrocytes (a type of nerve cell) and disrupts myelin production in the central nervous system. Myelin is the substance that helps form the brain’s white matter. It is made up of fats and proteins that form sheaths surrounding the fibrous parts of nerve cells. The myelin sheaths play an important role in the conduction of nerve impulses.

Scientists have discovered that the production of lamin B1 must be at just-right levels. If too much is produced it causes a distortion of the nuclear membrane, disruption of the nuclear pores, and altered chromosome structure. It appears that these effects lead to changes in the production of myelin proteins by altering gene expression. Without the proper levels of myelin proteins, the myelin sheaths don’t form correctly. This chain of events ultimately results in neurodegenerative disease (in this case, adult-onset autosomal dominant leukodystrophy).

Such precision and fine-tuning are not unusual in nature: they are hallmark features of nearly all biochemical systems. Moreover, they are also hallmark characteristics of intelligent design. Precision and fine-tuning dominate the best human designs and are often synonymous with exceptional quality. These properties do not arise by happenstance in either art or engineering. Rather, they come about only as a result of careful planning and a commitment to the best craftsmanship possible.

Similarly, nature’s no lemon. The molecular precision and fine-tuning that pervade the design of biochemical systems provide potent markers for the work of a Creator.

Endnotes
  1. Shu-Ting Lin and Ying-Hui Fu, “miR-23 Regulation of Lamin B1 is Crucial for Oligodendrocyte Development and Myelination,” Disease Models & Mechanisms 2 (Mar–Apr 2009): 178–88.

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  • Biochemical Design
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