R. G. Walker’s Paper Summery

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Sensation is converting physical stimuli into electrical currents, known as action potential (AP), via transduction; hence, scientists study extensively to find out the mechanism of transduction. However, no all is clear. In this paper, Dr. Walker and his colleagues studied mechanoreceptor mutated flies, with nompC gene (described in details in his paper) of NOMPC channel, and compared their channel domain of NOMPC with other organism.


Drosophila, the fly that Walker used to study, has very interesting mechanosensory bristle organ. Not only chemoreceptor but also mechanoreceptor attach to the dendrite, which directly connects to a hollow hair shaft. This hair shaft is able to sense the directional movements and the displacement; when the hair is compressed toward fly’s cuticle (Walker referred this as positive stimuli), the hair compresses the dendritic tip connected underneath and opens the transduction channels, creating action potential. More the hair moves toward its body, stronger the current goes through the channel. In addition, Walker found this response time is much faster than transduction of nd messenger cascades; therefore, the possibility of nd messenger transduction is eliminated.


Walker also found 4 types of defected nompC gene from fly mechanosensory mutants. Their genetic structures are very similar, yet the mechanoreceptor current (MCR) reading shows that adaptation is weaker than wild-type control. However, nompC4 plays an important role explaining transduction process. The nompC4 shows characteristic more similar to the control than other nompCs. Flies with nompC4 gene behave clumsier than wild-type, yet other nompCs show uncoordinated behavior. This suggests number of AP spikes, MRC, adaptation-time have direct behavior effect on organism. Molecular biology is very important tool to identify and extract the nompC gene from chromosome. Walker first mapped and rescued the gene from phenotype defected fly, used PCR to isolate the genes of nompCs. This shows NOMPC gene encodes a previously unidentified ion channels with a ANK repeats, which has about 40% similarity and 0% identical to TRP family of C. elegans.


From Walker and his colleagues’ paper, NOMPC plays a role as a mechanosensory transduction channel with evidences to support, such as nompC mutants have no mechanoreceptor responses, and single point mutation, nompC4, change the behavior of transduction. However, even though NOMPC and C. elegans’ TRP gene share 40% similarity, it is inefficient to be one of the evidence. This only suggests NOMPC derived from TRP family long time ago, but it doesn’t mean it still carries same function of transduction. Genetically, Chimp and human have % similarity, but two has very distinct physical differences and functions.


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Since fly does have NOMPC channels, what about higher developed vertebrate? As far as Walker found, vertebrate’s hair cells have homologues cell-signaling molecules. Farther studies can be done with vertebrates such as frogs, mice or even human. However, there may be some problems this similar experiment on vertebrate subjects. First, vertebrates are more sophisticated; mutant isolation may be difficult. Second, even if the precise mutant gene is isolated, similarity to NOMPC gene may be too low to be said they have any linkage. Last, there may not be a single point mutated gene, such as nompC4, in vertebrate hair cells. This may cause the experiment of finding NOMPC-like gene in vertebrate hair cells.


Many believe that sensory transduction will cause behavioral alternation, such as moths sense prey with their antenna in distant and fly in zigzags or dive to ground. Walker did a good job on nompC mutants study. One thing I did not understand fully is, how do the ANK repeats play an important role in this experiment, saying it suggests a new ion channel in Drosophila NOMPC gene? It seems NOMPC use ANK repeats to link to extracellular matrix; providing cell membrane sufficient tension to trigger ion channels.





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