It is hypothesized that motor proteins, dynein and kinesin control the transport of melanosomes into melanocyte dendrites as it is the net sum of cytoskeletal forces on an organelle that regulate intracellular transport. Dynein typically walk towards the minus-end of a microtubule in retrograde transport while kinesin move towards the plus-end in anterograde transport in neurons. The purpose of the article was to determine the role and effect of cytoplasmic dynein in melanosome transport in human melanocytes (1). Located in the basal layer of the epidermis, melanocytes produce melanin by inserting granules of melanin into melanosomes (2). Melanosomes are the site of synthesis, storage, and transport of melanin pigments that reside in the matrix
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The aim of the experiment was to determine if cytoplasmic dynein plays a role in retrograde melanosomal transport. The cell morphology and distribution of melanosomes appeared as black dots under a high-resolution time-lapse microscope. Panels A and C of Figure 7 are the negative sense DNA controls at 12 hours and 24 hours. Sense DNA melanocytes exhibited normal distribution around the nucleus. The antisense DNA at 12 hours in panel B and 24 hours in panel D show a change of peripheral distribution into complete dispersion of melanosomes in the cytoplasm. Antisense DNA in comparison to the dilute and sense DNA were more dispersed and showed anterograde motility while sense DNA showed retrograde motility (1). Normal cell function has perinuclear distributions and move towards the peripheral dendrites. Figure 8 relates to Figure 7 by supporting the claim that the pigment distribution of antisense DNA reduces from perinuclear distribution for a net increase of peripheral distribution of melanosomes. This was a gain of function experiment because nothing was removed from the melanosomes. Instead, the melanocytes in melanosomes were being treated with sense or antisense DNA. Secondary antibodies function to detect and visualize the first
The aim of the experiment was to determine if cytoplasmic dynein plays a role in retrograde melanosomal transport. The cell morphology and distribution of melanosomes appeared as black dots under a high-resolution time-lapse microscope. Panels A and C of Figure 7 are the negative sense DNA controls at 12 hours and 24 hours. Sense DNA melanocytes exhibited normal distribution around the nucleus. The antisense DNA at 12 hours in panel B and 24 hours in panel D show a change of peripheral distribution into complete dispersion of melanosomes in the cytoplasm. Antisense DNA in comparison to the dilute and sense DNA were more dispersed and showed anterograde motility while sense DNA showed retrograde motility (1). Normal cell function has perinuclear distributions and move towards the peripheral dendrites. Figure 8 relates to Figure 7 by supporting the claim that the pigment distribution of antisense DNA reduces from perinuclear distribution for a net increase of peripheral distribution of melanosomes. This was a gain of function experiment because nothing was removed from the melanosomes. Instead, the melanocytes in melanosomes were being treated with sense or antisense DNA. Secondary antibodies function to detect and visualize the first