Science Refutes Creationism

Information layers around information layers work like a data container https://medicalxpress.com/news/2017-10-important-mechanism-epigenetic-gene.html Excerpt: "How can defective gene activity leading to cancer be avoided? Researchers at the University of Zurich have now identified a mechanism by which cells pass on the regulation of genetic information through epigenetic modifications. These insights open the door to new approaches for future cancer treatments. ...Methylation marks on DNA act as molecular switches that regulate gene activity in order to coordinate the cell's specialization within the organism. How this DNA methylation is faithfully regulated, and how it can become defective, has not yet been fully resolved. However, the consequences are well known: In many cancer types, the methylation is deposited in the wrong place. This leads to genes being read incorrectly. Dual-layer epigenetic gene regulation Scientists at the University of Zurich have now found new pr

Lifestyle induced inheritable DNA mutations can be repaired on the atomic level https://www.broadinstitute.org/news/researchers-extend-power-gene-editing-developing-new-class-dna-base-editors Excerpt: "Scientists at Harvard University and the Broad Institute of MIT and Harvard have developed a new class of genome editing tool. This new “base editor” can directly repair the type of single-letter changes in the human genome that account for approximately half of human disease-associated point mutations. These mutations are associated with disorders ranging from genetic blindness to sickle-cell anemia to metabolic disorders to cystic fibrosis. The research team, led by David Liu, professor of chemistry and chemical biology at Harvard University, core institute member at the Broad Institute, and a Howard Hughes Medical Institute (HHMI) investigator, developed a molecular machine that can converts the DNA base pair A•T to G•C, without cutting the double helix, with high efficiency and

Lenski's long term experiments with bacteria contradict with evolutionary expectations http://www.newgeology.us/presentation32.html Excerpt: "You may have heard of the famous Lenski experiment. Dr. Richard E. Lenski is an evolutionary biologist who began a long-term experiment on February 24, 1988 that continues today. It looks for genetic changes in 12 initially identical populations of Escherichia coli bacteria that have been adapting to conditions in their flasks for over 60,000 generations. I have simplified a report by Scott Whynot, who studied 26 peer-reviewed scientific articles authored by Dr. Lenski (with others) published between 1991 and 2012. These papers represent the major genetic findings from 21 years of the experiment. 1. There was an insertion mutation that inhibited transcription of DNA involved in cell wall synthesis. 2. There was an insertion mutation in a regulatory region that encodes two proteins involved with cell wall synthesis. This may have led

Olfactory experience primes the heat shock transcription factor HSF-1 to enhance the expression of molecular chaperones in C. elegans https://medicalxpress.com/news/2017-10-worms-danger.html Excerpt: "Worms can learn. And the ways they learn and respond to danger could lead scientists to new treatments for people with neurodegenerative diseases. University of Iowa researchers researchers studied how roundworms—some of the most abundant animals on Earth—react to stressful situations by exposing them to the scent of a lethal bacterium. One group of roundworms exposed to the smell primed a defense mechanism that, when activated by stress, protected the worms' cells and increased the cells' survival. The group that wasn't exposed to the odor didn't prime its defense systems. When both groups were put in physical contact with the deadly bacterium, the roundworms that were exposed to the smell activated their cellular defenses more quickly, and more survived. The finding

Cohesin and Mediator protein complexes regulate cell type specific DNA loop structures to control gene expression http://wi.mit.edu/news/archive/2010/surprise-genome-structure-linked-developmental-diseases Excerpt: "Each cell type, such as skin cells, nerve cells, or embryonic stem cells, has its own gene expression program to maintain its cell state. For gene activation, transcription factors and gene expression machinery (RNA polymerase), bound to two different parts of the DNA called the promoter and the enhancer, must come in contact. This contact, which is facilitated and maintained by protein complexes called Mediator and Cohesin, forms a set of DNA loops that is specific to each cell type. Problems with this DNA loop structure can interfere with the activation of cell-type-specific genes, which can cause the cell to lose its normal state. Indeed, mutations in Mediator and Cohesin, the protein complexes that contribute to DNA loop formation, at cell-type-specific genes, can