Molecular and cellular characterization of GA-Stimulated Transcripts GASA4 and GASA6 in Arabidopsis thaliana.

GA and ABA play antagonistic roles in numerous cellular processes essential for growth, development, and stress responses. GASA4 and GASA6 belong to a family of GA-Stimulated transcripts in Arabidopsis, known as GA-inducible and ABA-repressible. We have found that GASA4 and GASA6 expression is likely mediated through a repressor of GA responses, GA INSENSITIVE (GAI) protein.

The Arabidopsis tandem zinc finger protein AtTZF1 affects ABA- and GA-mediated growth, stress and gene expression responses.

Tandem zinc finger (TZF) proteins are characterized by two zinc-binding CCCH motifs arranged in tandem. Human TZFs such as tristetraproline (TTP) bind to and trigger the degradation of mRNAs encoding cytokines and various regulators. Although the molecular functions of plant TZFs are unknown, recent genetic studies have revealed roles in hormone-mediated growth and environmental responses, as well as in the regulation of gene expression.

The Arabidopsis tandem zinc finger protein AtTZF1 traffics between the nucleus and cytoplasmic foci and binds both DNA and RNA.

Processing bodies (PBs) are specialized cytoplasmic foci where mRNA turnover and translational repression can take place. Stress granules are related cytoplasmic foci. The CCCH tandem zinc finger proteins (TZFs) play pivotal roles in gene expression, cell fate specification, and various developmental processes.

The CREB/CRE transcriptional pathway: protection against oxidative stress-mediated neuronal cell death.

Formation of reactive oxygen and nitrogen species is a precipitating event in an array of neuropathological conditions. In response to excessive reactive oxygen species (ROS) levels, transcriptionally dependent mechanisms drive the up-regulation of ROS scavenging proteins which, in turn, limit the extent of brain damage. Here, we employed a transgenic approach in which cAMP-response element binding protein (CREB)-mediated transcription is repressed (via A-CREB) to examine the contribution of the CREB/cAMP response element pathway to neuroprotection and its potential role in limiting ROS toxicity.