July 16, 2007 | David F. Coppedge

Cool Cell Tricks

Some cell parts act like acrobats, some like rescue workers, and some like I.T. professionals.  Here are some recent stories about the tricks that living cells perform each day.

  1. Precision formation flying:  The Scientist expressed amazement at the precision of key factors in development of the body plan in fruit flies.  The levels of expression in the bicoid factor “suggest a surprising level of accuracy in regulation of protein controlling body plan development.”  Words like “stunning,” “surprising” and “more complicated than we think” season the article.  “It’s very difficult to imagine how this could work,” said one.  The original papers on this process were published in Cell and summarized in a review article by Matthew Gibson.1
        A press release from Princeton elaborated on the precision of this process.  During development, it says, “cells make decisions to become one part of the body or another by a process so precise that they must be close to counting every available signaling molecule they receive from the mother.”  The article also says, “This signaling requires a sensitivity approaching the limits set by basic physical principles.”  One result of being able to measure things in biology these precisely was mentioned in the first paragraph: these are “discoveries that could change how scientists think not just about flies, but about life in general.”  The press release mentioned nothing about evolution.
  2. Chromosome triage:  Cells maintain a special “chromosome glue” called cohesin that can repair damaged DNA and keep sister chromatids together during cell division, reported EurekAlert.  The repair kit comes ready for emergencies: “Their results show that DNA damage can reactivate cohesin, which runs counter to the commonly held view that cohesion only arises during the DNA copying that takes place before cell division.”
        A paper on DNA repair was published in Nature last month,2 titled, “Chromatin dynamics and the preservation of genetic information.”  After mentioning the harm that can come from double-stranded breaks in DNA, the abstract said, “Recent work indicates that chromatin – the fibres into which DNA is packaged with a proteinaceous structural polymer – has an important role in initiating, propagating and terminating this cellular response to DNA damage.
        Science also chimed in on this subject, with a Perspectives article by Erwan Watrin and Jan-Michael Peters describing “How and why the genome sticks together.”3  Two papers in the issue give a new vista on the work a cell does to protect its library: “cohesion can be established in response to DNA damage independently of DNA replication,” they said.  “This overturns a long-held belief that cohesion is strictly coupled to DNA synthesis.  The papers also imply that DNA damage may have a broader impact than previously thought, triggering genomewide protection of chromosome integrity.
  3. Word processing foremen:  Non-coding sections of DNA may act as punctuation, an article on the Times Online reported.  This is further evidence that the concept of “junk DNA” is defunct. For years, evolutionary geneticists were puzzled by long stretches of apparently useless DNA: “This is puzzling, because scientists thought that evolution would fine-tune the human genome to preserve the essential bits and discard the rest,” wrote Anjana Ahuja for the Times. 

    Now an international team of scientists has discovered that junk DNA might regulate the activity of the genes they surround.  While genes do the hard work of making proteins, the junk DNA could be responsible for starting and stopping protein production.  “Some of the junk DNA might be considered punctuation markscommas and full stops that help make sense of the coding portion of the genome,” says Dr Victoria Lunyak, of the University of California, San Diego, School of Medicine, one of the authors of a paper published in Science.  Another analogy is to think of genes as building labourers, and the surrounding pieces of junk DNA as foremen.

    This almost makes it sound like the “junk DNA” is in some sense more important than the genes – that is, if managers are more important than laborers – a dubious proposition.

  4. Time to unwind:  A press release from Cornell shows an unwinding device at work: helicase, a molecular machine that unwinds DNA strands during replication.  “The research found that the helicase appears to actively exert a force onto the fork and separate the two strands,” the article said.  This shows that helicase is not a passive device.  It really works at its vital job.
  5. A bouquet with love:  You may have heard of telomeres, the tips of chromosomes, as mere caps on DNA to keep it from unraveling.  Cell published a new study that shows that these DNA ends organize into a “bouquet” that is essential for spindle pole formation during meiotic cell division.4  The authors said, “This discovery illuminates an unanticipated level of communication between chromosomes and the spindle apparatus that may be widely conserved among eukaryotes.”
  6. Talk to me:  The phenomenon of cell communication is a huge area of study.  Science Daily reported a finding that red blood cells “talk” to platelets, and that disruption of this communication leads to diabetes and heart attacks.
        In Current Biology,5 Paul Jarvis wrote about the “backchat” that goes on between chloroplasts and the nucleus in plant cells.  He assumed that chloroplasts evolved as once free-living cells that were engulfed by an ancestral prokaryote, and that their separate genomes were partitioned, most of the DNA going to the nucleus of the host.  Still, a remarkable degree of communication is required to ensure the proper amounts of chloroplast proteins are produced in the nucleus: “To ensure the correct, stoichiometric assembly of these complexes, and to enable their rapid reorganization in response to developmental or environmental cues, the activities of the nuclear and chloroplast genomes must be synchronized through intracellular signalling,” he said.  Each protein must then traverse the inner and outer membranes of the chloroplast, assisted by complexes of molecular machines.  Jarvis presented one example of the complexity involved in signalling:

    A particularly nice example is provided by the plastid protein import 1 (ppi1) mutant, which lacks the chloroplast protein import receptor atToc33.  This is actually one of two similar receptors in Arabidopsis, the other being atToc34, which are thought to have distinct substrate preferences: atToc33 mediating the import of the highly abundant precursors of the photosynthetic apparatus, and atToc34 the import of ‘housekeeping’ proteins (for example, components of the plastid’s genetic system, or enzymes of non-photosynthetic metabolism).  Remarkably, the ppi1 mutation triggers the specific down-regulation of photosynthesis-related genes (Figure 2), suggesting that retrograde signalling mechanisms exist to prevent the futile expression of proteins not able to reach their final, organellar destination.  Clearly, such exquisite regulation specificity could not be achieved were all plastid signalling pathways to converge and control gene expression through a common process.

    He did not elaborate on how all this “organellar repartee” could have evolved, though.  He just ended on the note, “Observations such as these suggest that a great deal remains to be learnt concerning plastid-to-nucleus signalling.”

  7. We brake for spindles:  Kinesin is usually thought of a molecular motor that power-walks down a track.  But what good is an engine without a brake?  When kinesin needs to carry a load, or when it needs to winch apart chromosomes during cell division, something needs to tell it when to stop.  An article in Current Biology6 shows that in some cases, kinesin-5 has a built-in braking mechanism:

    Faithful chromosome segregation depends upon the formation and function of a bipolar, microtubule (MT)-based mitotic spindle, which uses multiple mitotic motors to assemble itself and to separate sister chromatids.  Among these motors, members of the kinesin-5 family are thought to have critical and often essential mitotic functions, by pushing apart the spindle poles, for example during anaphase B spindle elongation.  Curiously, however, the single kinesin-5 present in Caenorhabditis elegans, BMK-1, is dispensible for mitosis.  Now, new work from the Saxton and Strome laboratories, published recently in Current Biology, shows that, in this system, BMK-1 has novel mitotic functions, serving as a brake that restrains the rate of anaphase spindle-pole separation driven by other cortical force generators.

    The authors thought it “somewhat surprising to find such distinct, indeed opposite, roles for kinesin-5, acting as a brake on ipMT sliding in the spindles of C. elegans embryos versus actively pushing apart ipMTs in spindles of other systems, such as Drosophila embryos.”  More work is being done to figure out how this is possible.

None of these papers explained how evolution could come up with the tricks.  The last entry, though, simply stated as a matter of fact that natural selection did it somehow.  Still, the authors’ astonishment at the diversity and complexity of molecular motors left it challenging to believe it all just happened:

Some of us recall the time when the world of motor proteins seemed relatively uncomplicated; cilia used dynein, muscles used myosin, and we sensed that the discovery of ‘THE mitotic motor’ lay just around the corner.  Subsequently, mitosis researchers have uncovered a far more fascinating scenario in which multiple mitotic motors, a dozen or so in Drosophila for example, are deployed to functionally coordinate the highly choreographed sequence of motility events associated with spindle assembly and chromatid separation.  The work of Saunders et al.  on kinesin-5 extends our growing appreciation of mitotic motor diversity by suggesting that this key mitotic motor can be used to carry out a previously unrecognized function in C. elegans spindles.  As these authors point out, it is striking how natural selection adopts such diverse strategies in different cell-types to move apart sister chromatids the few microns required to ensure that the products of each cell division inherit a complete set of genetic instructions.  This diversity presents a challenge, since useful general models for spindle assembly and function must not only incorporate the basic principles common to all spindles, but should also be sufficiently adaptable to encompass the diversity of spindle design produced by natural selection.


1Matthew Gibson, “Bicoid by the Numbers: Quantifying a Morphogen Gradient,” Cell, Volume 130, Issue 1, 13 July 2007, pages 14-16, doi:10.1016/j.cell.2007.06.036.
2Jessica A. Downs, Michel C. Nussenzweig and Andre Nussenzweig, “Review article: Chromatin dynamics and the preservation of genetic information,” Nature 447, 951-958 (21 June 2007) | doi:10.1038/nature05980.
3Erwan Watrin and Jan-Michael Peters, “Molecular Biology: How and When the Genome Sticks Together,” Science, 13 July 2007: Vol. 317. no. 5835, pp. 209-210, DOI: 10.1126/science.1146072.
4Kazunori Tomita and Julia Promisel Coope, “The Telomere Bouquet Controls the Meiotic Spindle,” Cell, Volume 130, Issue 1, 13 July 2007, pages 113-126, doi:10.1016/j.cell.2007.05.024.
5Paul Jarvis, “Intracellular Signalling: Chloroplast Backchat,” Current Biology, Volume 17, Issue 14, 17 July 2007, Pages R552-R555, doi:10.1016/j.cub.2007.05.021.
6Gul Civelekoglu-Scholeya and Jonathan M. Scholey, “Mitotic Motors: Kinesin-5 Takes a Brake,” Current Biology, Volume 17, Issue 14, 17 July 2007, Pages R544-R547, doi:10.1016/j.cub.2007.05.030.

We must continue to juxtapose the unfolding intricacies of cellular machinery with the farcical explanations proposed by evolutionists.  Darwinian thinking is so entrenched, only repeated application of detailed instances as shown above can produce the cumulative effect on brainwashed minds that is obvious to the rest of us: trying to explain these wonders by unguided processes of mindless evolution is just plain dumb.  Some day, this will be obvious to everybody.  Future biologists will look back with bewilderment that so many smart people fell for such silly notions for so long.  They will understand intuitively that quality control, effective communication and choreographed performances are hallmarks of planning, guidance, and intelligence.  How could anyone have thought otherwise?  Someone’s motors weren’t turning, for sure.

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