bZIP transcription factor interactions regulate DIF responses inDictyostelium

Abstract

The signalling molecule DIF-1 is required for normal cell fate choice and patterning in Dictyostelium. To understand how these developmental processes are regulated will require knowledge of how cells receive and respond to the DIF-1 signal. Previously, we have described a bZIP transcription factor, DimA, which is required for cells to respond to DIF-1. However, it was unknown whether DimA activity is required to activate the DIF response pathway in certain cells or is a component of the response pathway itself. In this study, we describe the identification of a DimA-related bZIP transcription factor, DimB. Rapid changes in the subcellular localisation of both DimA and DimB in response to DIF-1 suggest that they are directly downstream of the DIF-1 signal. Genetic and biochemical interactions between DimA and DimB provides evidence that their ability to regulate diverse targets in response to DIF-1 is partly due to their ability to form homo-and heterodimeric complexes. DimA and DimB are therefore direct regulators of cellular responses to DIF-1.

The Inositol 1,4,5-Trisphosphate Receptor Is Required to Signal Autophagic Cell Death

“…The iplA Ϫ mutation prevented cellulose shell synthesis around cells subjected to DIF, consistent with control by IP3R and Ca 2ϩ flux of the expression of genes governing cellulose synthesis. Moreover, addition of DIF triggered nuclear accumulation of DimA, and also of DimB, a second bZIP transcription factor, within a few minutes in AX2 and AX4 strains (Huang et al, 2006;Zhukovskaya et al, 2006). Interestingly, DimB was required for vacuolar cell death and repression of nonvacuolar cell death in response to DIF (Huang et al, 2006), like Atg1.…”

“…Moreover, addition of DIF triggered nuclear accumulation of DimA, and also of DimB, a second bZIP transcription factor, within a few minutes in AX2 and AX4 strains (Huang et al, 2006;Zhukovskaya et al, 2006). Interestingly, DimB was required for vacuolar cell death and repression of nonvacuolar cell death in response to DIF (Huang et al, 2006), like Atg1. Together, these data support the idea that DIF could trigger ACD by activating transcription factors through the IP3R/Ca 2ϩ pathway.…”

A necrotic cell death model in a protist

“…When added after a 4 h starvation period, DIF led within 2-3 min to the tyrosine phosphorylation of the STATc transcription factor, 21 thus detectably preventing the exit of STATc from the nucleus, 22 and induced changes in subcellular localization of the transcription factor DimB. 23,24 The relationship between DIF-induced rapid phosphorylation events and DIF-induced rapid uncoupling of oxidative phosphorylation is not known.…”

What can microbial genetics teach sociobiology?

“…The answer, at least in part, is pleiotropy. The gene dimA is central to the response of prestalk cells to DIF-1, and a mutant with this gene knocked out creates cells that behave like cheaters and preferentially become prespore cells in slugs when mixed with wild-type cells [53][54][55]. However, another effect of inactivating dimA ultimately prevents cheating: the ability of cells to enter the spore head of the fruiting body and produce spores is inhibited [53].…”