Figure 2.

Genetic analyses of Mist1/DIMM functions reveal their scaling factor properties.

Top: A schematic of results observed in a MIST1 loss of function model [3]. During normal zymogenic chief cell development, the chief cell begins to express MIST1 as it arises from its mucous granule-containing neck cell precursor. MIST1 is required for the expansion of apical cytoplasm and formation/maintenance of large, zymogenic vesicles. In its absence, cell apices are stunted, vesicles are smaller, and nuclei are nearer the cell apex.

Bottom: A schematic of results observed in a DIMM gain of function model [17].

Drosophila photoreceptors project axons that terminate within the brain, and store the fast neurotransmitter histamine within small clear synaptic vesicles (SSV). SSVs are released from T-bar type active zones (AZ) and retrieved by endocytosis at glia invaginations – capitate projections (CP). Following mis-expression of DIMM at moderate (top) or high (bottom) levels), the properties of the photoreceptor are transformed. Low-level DIMM mis-expression results in accumulation of small dense-core vesicles (Small DCV) in addition to the SSV. Hi-level DIMM mis-expression results in loss of SSVs, AZs and CPs, and the heavy accumulation of large DCVs. With co-mis-expression of a neuropeptide precursor transgene, the large DCVs process and store mature neuropeptide.