<Li> Strengths: This model is consistent with numerous observations and encompasses some of the strengths of the cisternal progression / maturation model . Additionally, what is known of the Rab GTPase roles in mammalian endosomes can help predict putative roles within the Golgi . This model is unique in that it can explain the observation of "megavesicle" transport intermediates . </Li> <Li> Weaknesses: This model does not explain morphological variations in the Golgi apparatus, nor define a role for COPI vesicles . This model does not apply well for plants, algae, and fungi in which individual Golgi stacks are observed (transfer of domains between stacks is not likely). Additionally, megavesicles are not established to be intra-Golgi transporters . </Li> <P> Though there are multiple models that attempt to explain vesicular traffic throughout the Golgi, no individual model can independently explain all observations of the Golgi apparatus . Currently, the cisternal progression / maturation model is the most accepted among scientists, accommodating many observations across eukaryotes . The other models are still important in framing questions and guiding future experimentation . Among the fundamental unanswered questions are the directionality of COPI vesicles and role of Rab GTPases in modulating protein cargo traffic . </P> <P> Brefeldin A (BFA) is a fungal metabolite used experimentally to disrupt the secretion pathway as a method of testing Golgi function . BFA blocks the activation of some ADP - ribosylation factors (ARFs). ARFs are small GTPases which regulate vesicular trafficking through the binding of COPs to endosomes and the Golgi . BFA inhibits the function of several guanine nucleotide exchange factors (GEFs) that mediate GTP - binding of ARFs . Treatment of cells with BFA thus disrupts the secretion pathway, promoting disassembly of the Golgi apparatus and distributing Golgi proteins to the endosomes and ER . </P>

What is the appearance of the golgi apparatus