High impact information on jing

• Loss of jing-lacZ expression in homozygous sim mutants and induction of jing-lacZ by ectopic sim expression establish that jing is part of the CNS midline lineage [1].
• In jing homozygous mutant embryos, reductions in marker gene expression and inappropriate apoptosis in the CNS midline and trachea establish that jing is essential for the proper differentiation and survival of these lineages [1].
• Given the similarities between JING and the vertebrate CCAAT-binding protein AEBP2, we propose that jing regulates transcriptional mechanisms in Drosophila embryos and promotes cellular differentiation in ectodermal derivatives [1].
• We have isolated embryonic recessive lethal jing mutations that display genetic interactions in the embryonic CNS midline and trachea, with mutations in the bHLH-PAS genes single-minded and trachealess, and their downstream target genes (slit and breathless) [1].
• The jing mutant phenotype resembles that of slbo mutations, which disrupt the Drosophila C/EBP gene, but is distinct from other classes of border cell migration mutants [2].

Biological context of jing

• Loss- and gain-of-function studies have demonstrated a crucial role for the jing zinc finger transcription factor in neuronal and glial differentiation and survival in the embryonic central nervous system midline of Drosophila [3].
• We further find that jing is required for neuronal and glial survival as repo- and castor-expressing cells undergo cell death in homozygous jing (3) mutant embryos, as revealed by double labeling with Tunel [3].
• The jing locus was identified in a screen for mutations that cause border cell migration defects in mosaic clones [2].
• We establish that the jing zinc-finger transcription factor plays an essential role in controlling CNS midline and tracheal cell differentiation. jing transcripts and protein accumulate from stage 9 in the CNS midline, trachea and in segmental ectodermal stripes [1].
• Together, these results show that jing regulates signal transduction in developing midline and tracheal cells [4].

Anatomical context of jing

• The jing Zn-finger transcription factor is a mediator of cellular differentiation in the Drosophila CNS midline and trachea [1].

Other interactions of jing

• Interestingly, we also demonstrate that two other genes affecting alula development, Alula and elbow, also exhibit tsh derepression in the same region of the wing disc as jing- clones [5].
• In addition, circumesophageal connectives are repelled after expression of two copies of UAS- jing in sim-expressing cells, suggesting the activation of axon repellent molecules [3].
• Together, our data suggest that jing encodes a transcriptional repressor that may participate in a subset of Pc-dependent activities during Drosophila appendage development [5].
• Activation of the Egfr pathway in loss-of-function jing mutants partially rescues midline cell loss [4].
• The jing and ras1 pathways are functionally related during CNS midline and tracheal development [4].

References