Disease relevance of pspG

• In the TRAP1-RNAi cells, PSV formation and therefore prespore differentiation were significantly impaired, particularly under a heat stress condition [1].
• The 85-kDa PL3 protein synthesized in vivo accumulates specifically in regulated secretory vesicles of prespore cells (prespore vesicles), as determined microscopically using antibody against a PL3 gene fusion product expressed in Escherichia coli [2].

High impact information on pspG

• The 2.2 kb mRNA of the Dictyostelium discoideum prespore gene EB4-PSV is constitutively transcribed during growth and development, but the message is only accumulated when cells form aggregates and establish the prespore-prestalk pattern [3].
• Using poly(A+) RNA from the fractionated cells to probe a cDNA library of mRNAs from postaggregation cells, we were able to identify six cDNA clones representing RNAs enriched in prespore or prestalk cells [4].
• The prestalk gene, pst-cathepsin, encodes a protein highly homologous to the lysosomal cysteine proteinases cathepsin H and cathepsin B. The prespore gene encodes a protein with some homology to the anti-bacterial toxin crambin and has been designated beejin [5].
• Discoidin II became prominent later and ultimately localized in what appear to be prespore vesicles [6].
• Neutral red-stained anterior-like cells in the prespore zone of slugs move straight forward in the direction of slug migration and, furthermore, show coherent periodic cell movement [7].

Biological context of pspG

• cAMP induction of prespore and prestalk gene expression in Dictyostelium is mediated by the cell-surface cAMP receptor [8].
• The cell movement data show that the chemotactic signal in the slug propagates as a three-dimensional scroll wave in the prestalk zone and as a planar wave in the prespore zone [7].
• In cells disaggregated in the absence of cyclic AMP, all prestalk and prespore mRNAs decayed with biphasic kinetics [9].
• Initial prestalk and prespore cell differentiation did not seem to be compromised in the mutant since the expression of several cell-type-specific markers were found to be unaffected [10].
• Our results suggest that psi factor plays important roles not only in prespore cell differentiation but also in the progress of the cell cycle in the prespore pathway in normal development [11].

Anatomical context of pspG

• At least three distinct types of cell arise from a population of similar amoebae during Dictyostelium development: prespore, prestalk A and prestalk B cells [12].
• Prespore vacuoles (PSVs) are specifically formed in prespore cells of the cellular slime moulds and contain spore-specific antigens [13].
• Moreover, a similar pattern of changes in the Golgi apparatus and related structures occurs during the re-differentiation of prespore cells within prestalk isolates [13].
• We found that the PsB complex first accumulates in prespore vesicles in slug cells and is secreted later during culmination and becomes localized to both the extracellular matrix of the apical spore mass of mature fruiting bodies and to the inner layer of the spore coat [14].
• We have previously demonstrated that Dictyostelium discoideum TRAP1 (Dd-TRAP1) synthesized at the vegetative growth phase is retained during the whole course of D. discoideum development, and that at the multicellular slug stage, it is located in prespore-specific vacuoles (PSVs) of prespore cells as well as in the cell membrane and mitochondria [1].

Associations of pspG with chemical compounds

• In the presence of conditioned medium factor(s), exogenous cyclic AMP at the onset of starvation fails to induce the prespore and prestalk genes [15].
• The Dictyostelium discoideum cell surface antigen PsA is a glycoprotein which first appears in the multicellular stage soon after tip formation and is selectively expressed on prespore cells [16].
• (i) Only cAR1 can mediate adenosine inhibition of cAMP-induced prespore gene expression, a phenomenon that was found earlier in wild-type cells. cAR1's mediation of adenosine inhibition suggests that cAR1 normally mediates prespore gene induction [17].
• Incubating disaggregated cells with daunomycin to inhibit RNA synthesis prevented the loss of prespore mRNAs, whereas the inhibitor decreased or did not affect levels of the common mRNAs CZ22 and actin [18].
• Cycloheximide, which inhibited protein synthesis almost completely, prevented the loss of the prespore mRNAs, but puromycin, which inhibited protein synthesis less well, did not [18].

Regulatory relationships of pspG

• The absence of an apparent gradient of staining in these structures suggest that PKA is equivalently activatable throughout the prespore region and that all prespore cells are competent to express spiA [19].
• Further, induced transdifferentiation of prespore cells into prestalk cells is inhibited in rzpA-slugs [20].
• The behavior of these cis-regulatory elements implies that the mechanism regulating the prespore-specific expression of rnrB is different from that regulating other known prespore genes [21].
• Disruption of the cell-fate gene stkA leads to a phenotype in which all the cells destined to become spores end up as stalk cells. 'Stalky' mutants express normal levels of prespore cell transcripts but fail to produce the culmination-stage spore transcript spiA [22].
• A novel prespore-cell-inducing factor in Dictyostelium discoideum induces cell division of prespore cells [11].

Other interactions of pspG

• spiA, a marker for sporulation, is expressed during the culmination stage of Dictyostelium development, when the mass of prespore cells has moved partly up the newly formed stalk [19].
• Disruption of the rZIP gene rzpA results in altered cellular aggregation, impaired slug migration, and aberrant patterning of prespore and prestalk cells, the major progenitor classes [20].
• During slug migration they are replaced by a band of ecmB-expressing cells, situated in the front half of the prespore zone and tightly apposed to the substratum [23].
• Expression of the mutant G alpha 2 from the SP60 prespore promoter or wild-type G alpha 2 from either the ecmA or the SP60 promoter results in no detectable phenotype [24].
• Participation in the prespore/spore population returns with the restoration of a modified pdsA to the null cells [25].

Analytical, diagnostic and therapeutic context of pspG

• Prespore and prestalk cells in Dictyostelium discoideum aggregates can be separated by density gradient centrifugation [4].
• Immunoblot analysis and cell-by-cell double-label immunofluorescence of these mixtures showed that mutant cells underproduced several prespore cell markers [26].
• Dual parameter flow cytometry was used to demonstrate that the 117 antigen is found on the surface of maturing prespore cells after the PsA glycoprotein disappears, but that it is not found on mature spores [27].
• The apparent deterioration of the prestalk/prespore pattern in older slugs is thus an artefact of reporter stability [28].
• We have examined the processes of PSV formation in Dictyostelium discoideum, using both the methods of immunoelectron microscopy with antispore serum and electron-microscopic radioautography with [3H]fucose, which is specifically incorporated into prespore cells [13].

References