Information is the stuff of life. Not limited to DNA, information is found in most biomolecules in living cells. Here are some recent developments.
Certain forms of sugars (polysaccharides called chitosans) trigger the immune system of plants. Biologists at the University of Mnster are deciphering the sugar code. They describe the variables in chitosans that constitute a signaling system.
Chitosans consist of chains of different lengths of a simple sugar called glucosamine. Some of these sugar molecules carry an acetic acid molecule, others do not. Chitosans therefore differ in three factors: the chain length and the number and distribution of acetic acid residues along the sugar chain. For about twenty years, chemists have been able to produce chitosans of different chain lengths and with different amounts of acetic acid residues, and biologists have then investigated their biological activities. [Emphasis added.]
These polysaccharides, also found in animals, are perhaps the most versatile and functioning biopolymers, the scientists say. If they can learn to decipher this complex code, they might find ways to protect plants without the use of pesticides.
DNA is becoming known as a more of a team member in a society of biomolecules. In some ways, it is more a patient than a doctor. It gets operated on by numerous machines that alter its message. One of the most important doctors that operates on RNA transcripts is the spliceosome, says a review article in The Scientist about alternative splicing. This complex molecular machine can multiply the messages in the coding regions of DNA by cutting out introns and stitching coded parts called exons together in different ways.
The process of alternative splicing, which had first been observed 26 years before the Human Genome Project was finished, allows a cell to generate different RNAs, and ultimately different proteins, from the same gene. Since its discovery, it has become clear that alternative splicing is common and that the phenomenon helps explain how limited numbers of genes can encode organisms of staggering complexity. While fewer than 40 percent of the genes in a fruit fly undergo alternative splicing, more than 90 percent of genes are alternatively spliced in humans.
Astoundingly, some genes can be alternatively spliced to generate up to 38,000 different transcript isoforms, and each of the proteins they produce has a unique function.
The discovery of splicing seemed bizarre from an evolutionary perspective, the authors say, recalling obsolete ideas about junk DNA. It seemed weird and wasteful that introns were being cut out of transcripts by the spliceosome. Then, the ENCODE project found that the vast majority of non-coding DNA was transcribed, giving these seemingly nonfunctional elements an essential role in gene expression, as evidence emerged over the next few years that there are sequences housed within introns that can help or hinder splicing activity.
This article is a good reminder that evolutionary assumptions hinder science. Once biochemists ridded themselves of the evolutionary notion of leftover junk in the genetic code, a race was on to understand the role of alternative splicing.
Understanding the story behind each protein in our bodies has turned out to be far more complex than reading our DNA. Although the basic splicing mechanism was uncovered more than 40 years ago, working out the interplay between splicing and physiology continues to fascinate us. We hope that advanced knowledge of how alternative splicing is regulated and the functional role of each protein isoform during development and disease will lay the groundwork for the success of future translational therapies.
Another discovery that is opening doors to research opportunities comes from the University of Chicago. Darwin-free, they announce a fundamental pathway likely to open up completely new directions of research and inquiry. Biologists knew about how methyl tags on RNA transcripts regulate the ways they are translated. Now, Professor Chuan He and colleagues have found that some RNAs, dubbed carRNAs, dont get translated at all. Instead, they controlled how DNA itself was stored and transcribed.
This has major implications in basic biology, He said. It directly affects gene transcriptions, and not just a few of them. It could induce global chromatin change and affects transcription of 6,000 genes in the cell line we studied.
Dr. He is excited about the breakthrough. The conceptual change in how RNA regulates DNA offers an enormous opportunity to guide medical treatments and promote health. Take a look at this design-friendly quote:
The human body is among the most complex pieces of machinery to exist. Every time you so much as scratch your nose, youre using more intricate engineering than any rocket ship or supercomputer ever designed. Its taken us centuries to deconstruct how this works, and each time someone discovers a new mechanism, a few more mysteries of human health make sense and new treatments become available.
Remember the evolutionary myth that jumping genes were parasites from our evolutionary past that learned how to evade the immune system? A discovery at the Washington University School of Medicine changes that tune, saying, Jumping genes help stabilize DNA folding patterns. These long-misunderstood genes thought by some evolutionists to be sources of novel genetic traits actually function to provide genomic stability.
Jumping genes bits of DNA that can move from one spot in the genome to another are well-known for increasing genetic diversity over the long course of evolution. Now, new research at Washington University School of Medicine in St. Louis indicates that such genes, also called transposable elements, play another, more surprising role: stabilizing the 3D folding patterns of the DNA molecule inside the cells nucleus.
It appears that by moving around, these genes can preserve the structure of DNA while not altering its function. (Note: the evolution they speak of appears to be microevolution, which is not controversial; hear Jonathan Wells discuss this on ID the Future.)
According to the researchers, this redundancy makes the genome more resilient. In providing both novelty and stability, jumping genes may help the mammalian genome strike a vital balance allowing animals the flexibility to adapt to a changing climate, for example, while preserving biological functions required for life.
Lead author Ting Wang says this gives insight into why coding regions between different animals vary in structure.
Our study changes how we interpret genetic variation in the noncoding regions of the DNA, Wang said. For example, large surveys of genomes from many people have identified a lot of variations in noncoding regions that dont seem to have any effect on gene regulation, which has been puzzling. But it makes more sense in light of our new understanding of transposable elements while the local sequence can change, but the function stays the same.
So while evolutionists had expected junk and simplicity, Wang says the opposite has occurred. We have uncovered another layer of complexity in the genome sequence that was not known before. Now, more discoveries are likely to flow from intelligent designs expectation that a closer look reveals more complexity.
In another recent podcast at ID the Future honoring the late Phillip E. Johnson, Paul Nelson likened a graph of mounting discoveries about life to a sharply rising mountain range. Darwin proposed his theory on the flatlands, unaware of the peaks his theory would have to explain. In the last fifty years, scientists have encountered mountain after mountain of complexity in life that evolutionary theory never anticipated back out there on the flatlands. We cant see the top of the mountains yet, but we know that were still not there, and we wont be for a long, long time, Nelson says. As we witness scientists continuing up the mountains, we anticipate with awe more wonders of design that will likely come to light in the next decade.
Image: Interior of a cell, courtesy of Illustra Media.
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Surprises in Cell Codes Reveal Information Goes Far Beyond DNA - Discovery Institute
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