triggers exocytosis might interact either with the SNARE complex or with the phospholipids of the fusing membranes. Synaptotagmin has been recognized as the major sensor for Ca2+ triggered exocytosis in animals. However, synaptotagmin proteins are absent in plants and unicellular eukaryotes. Other potential calcium sensors for exocytosis are EF-hand proteins (Ex: Calmodulin) and C2-domain (Ex: Ferlins, E-synaptotagmin, Doc2b) containing proteins. It is unclear how the differenta calcium sensors can cooperate together and mediate the calcium triggered exocytosis kinetic in a specific fashion. Constitutive exocytosis is performed by all cells and serves the release of components of the extracellular matrix or delivery of newly synthesized membrane proteins that are incorporated in the plasma membrane after the fusion of the transport vesicle. There is no clear consensus about the machinery and molecular processes that drive the formation, budding, translocation and fusion of the post-Golgi vesicles to the plasma membrane. The fusion involves membrane tethering (recognition) and membrane fusion. It is still unclear if the machinery between the constitutive and regulated secretion is different. The machinery required for constitutive exocytosis hasn’t been studying as much as the mechanism of regulated exocytosis. Two tethering complexes are associated with constitutive exocytosis in mammals, ELKS and Exocyst. ELKS is a large coiled-coil protein, also involved in synaptic exocytosis, marking the ‘hotspots’ fusion points of the secretory carriers fusion. Exocyst is an octameric protein complex. In mammals, exocyst components localize in both plasma membrane, and Golgi apparatus and the exocyst proteins are colocalized at the fusion point of the post-Golgi vesicles. The membrane fusion of the constitutive exocytosis, probably, is mediated by SNAP29 and Syntaxin19 at the plasma membrane and YKT6 or VAMP3 at the vesicle membrane. Vesicular exocytosis in prokaryote gram negative bacteria is a third mechanism and latest finding in exocytosis. The periplasm is pinched off as bacterial outer membrane vesicles (OMVs) for translocating microbial biochemical signals into eukaryotic host cells or other microbes located nearby, accomplishing control of the secreting microbe on its environment - including invasion of host, endotoxemia, competing with other microbes for nutrition, etc. This finding of membrane vesicle trafficking occurring at the host-pathogen interface also dispels the myth that exocytosis is purely a eukaryotic cell phenomenon. Steps Five steps are involved in exocytosis: Vesicle trafficking Certain vesicle-trafficking steps require the transportation of a vesicle over a moderately small distance. For example, vesicles that transport proteins from the Golgi apparatus to