Silencing SCF affected paracrine factor expressions in the fibroblasts. Melanocytes receive the signals generated from fibroblasts and then activate melanin production. In subsequent experiments, we investigated whether SCF-silenced fibroblasts further influenced melanocytes for melanogenesis, and the gene expression in melanocytes was determined. Melanin biosynthesis is a complex process occurring in melanocytes within particular membrane-bound organelles, known as melanosomes . The major component of the melanosome is Pmel17, which is a transmembrane protein and essential for melanin synthesis and deposition to form the fibrillar matrix. Rab27a, melanophilin (MLPH), and Myo5a form a tri-protein complex to bind melanosomes at the melanocytes peripheries. In the process of melanosome transport, the ternary complex is the connection between actin cytoskeleton and melanosome. A lack of these proteins affects the transport, and melanoregulin (Mreg) drives melanosome transfer from melanocytes to keratinocytes via a regulated shedding mechanism. Human skin melanin is driven by the intercellular movement of melanin-containing melanosomes from the extremities of human melanocytes dendrites to neighboring keratinocytes. When it is carried by the actin filament, melanosome moves to the dendritic tail section, through exocytosis, and is transported into keratinocytes . The greater the amount of melanin that is transferred into keratinocytes, the darker is the color of the skin . The movement on the microtubule depends on the dynein–dynactin motor complex. Mreg forms a complex with Rab-interacting lysosomal protein and p150 (Glued), which is a subunit of dynactin . Mreg adjusts a shedding system which makes melanosome transport from human melanocytes to keratinocytes. The shedding process from human melanocytes of melanosome-rich packages is undergoing the phagocytosis of keratinocytes. The shedding not only takes place principally at dendritic extremities, but also around the center areas, having the adhesion to keratinocytes, tightening behind the forming packages, and apparent self-abscissions . The movement on the actin filament requires Myo5a, Rab27a, and MLPH as the connecting bridge . 36H downregulated protein expression for Myo5a and might prevent a darkening of skin color. Melanin is deposited on these fibers and melanosomes become mature in the melanocytes . Melanocytes are activated through multiple paracrine factors secreted from adjacent cells, such as keratinocytes and fibroblasts. The paracrine factors bind to the specific receptors expressed on melanocytes and then accelerate signal transductions to initiate melanin production. For example, SCF binds to the c-kit receptor, and MAPK family, ERK1/2, JNK, and p38, are activated in the melanocytes, thereby altering MITF activities and functions through phosphorylation or dephosphorylation. MITF is a specific transcription factor of tyrosinase, TRP-1 and TRP-2, and the mutant of MITF leads to a deficiency in melanocytes. Melanin is the end product of the multistep conversion of tyrosine. Tyrosinase, a rate-limiting enzyme, catalyzes tyrosine into DOPA, and subsequently DOPA undergoes a separate pathway to convert to pheomelanin or eumelanin. After maturation of melanin, it is transferred to keratinocytes along with microtubules and dendrites by the kinesin and dynein motor proteins. Actin-based motor protein myosinVa attaches to melanosomes and moves via interaction with Rab27a and melanophilin to the surrounding keratinocytes.