August 9, 2010 | David F. Coppedge

Specialized Molecules Make Cells Work

Reports continue to show that vital cell processes depend on finely-tuned proteins and RNA molecules.  Most of the papers that discuss these specialized molecules fail to mention how they might have evolved, as shown in three papers in the recent issue of Science.

  1. Walker with muscle:  A paper by Kaya and Higuchi from the University of Tokyo discussed how myosin motors, the active force-generating machines in muscle, adjust their walking steps with non-linear elasticity.1  Myosins work together in muscle.  Their ability to reduce stiffness and adjust their walk is essential: “the load-dependent changes in the step size are an essential property of skeletal myosin,” the authors said.  Their last sentence explained why this contributes to their effectiveness: “Such molecular properties may be inherent in the assembly of molecular motors and may reduce molecular interference, leading to the high mechanical efficiency of muscle contraction.”  You have your elastic myosins to thank for every simple or complex move you make.  For more stories about myosin this year, see 04/19/2010, 02/19/2010, and 01/19/2010.
  2. Junk with control:  It wasn’t long ago when any non-coding region of the genome was considered junk.  No longer; lincRNAs are emerging as stars of regulation and control (see 08/02/2010).  Another finding to that effect was published in Science by an international team from Stanford, Harvard and the Weizmann Institute in Israel.2  They studied one lincRNA called HOTAIR that has two specific binding domains for making histone modifications.  Histone is the protein on which DNA winds.  It contains molecular tags that affect translation – the “histone code” (see 12/22/2009, bullet 5, with its embedded links).
        The team found that HOTAIR, an RNA generated from non-coding DNA, is intimately involved with the regulation of histone by forming a scaffold for PRC2 and LSD1 proteins: “The functional consequence of coordinate targeting of PRC2 and LSD1 by HOTAIR is gene repression,” they said.  What they found may apply to other cases: “Some lincRNAs may be ‘tethers’ that recruit several chromatin modifications to their sites of synthesis while other lincRNAs can act on distantly located genes as ‘guides’ to affect their chromatin states,” the concluded.  “On the basis of their dynamic patterns of expression, specific lincRNAs can potentially direct complex patterns of chromatin states at specific genes in a spatially and temporally organized manner during development and disease states.”
  3. Repairmen with teamwork:  A team at Zheijiang University in China studied the partners in DNA interstrand cross-link repair, one of many repair pathways active in the genome.  Fanconi anemia is a disease caused by mutations in 13 Fanc genes.3    “Here, we characterize a previously unrecognized nuclease, Fanconi anemia?associated nuclease 1 (FAN1), that promotes ICL repair in a manner strictly dependent on its ability to accumulate at or near sites of DNA damage and that relies on mono-ubiquitylation of the ID complex,” they said, referring to the tagging of a repair site with ubiquitin, a “ubiquitous” cellular tag signaling a site for repair or demolition.  “Thus, the mono-ubiquitylated ID complex recruits the downstream repair protein FAN1 and facilitates the repair of DNA interstrand cross-links.”
        For more on DNA repair teams in the cell, see the 07/18/2001, 07/26/2002, 01/30/2003, 02/13/2004, 03/31/2005, 08/14/2007, and 03/14/2010 entries.

These three papers are examples of many that are continuously being published in leading journals that (1) explore highly-specific molecules involved in vital cellular processes and (2) say nothing about evolution.  Examples could be easily multiplied.


1.  Kaya and Higuchi, “Nonlinear Elasticity and an 8-nm Working Stroke of Single Myosin Molecules in Myofilaments,” Science, 6 August 2010: Vol. 329. no. 5992, pp. 686-689, DOI: 10.1126/science.1191484.
2.  Tsai, Manor et al, “Long Noncoding RNA as Modular Scaffold of Histone Modification Complexes,” Science, 6 August 2010: Vol. 329. no. 5992, pp. 689-693, DOI: 10.1126/science.1192002.
3.  Liu, Ghosai, Yuan, Chen and Huang, “FAN1 Acts with FANCI-FANCD2 to Promote DNA Interstrand Cross-Link Repair,” Science, 6 August 2010: Vol. 329. no. 5992, pp. 693-696, DOI: 10.1126/science.1192656.

Who needs evolution?  Not these authors.  Not medical science, genetics, or cell biology, either.  Let’s move along, and leave Darwinism to rust in pieces.

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