Tenascin major


REGULATION

Transcriptional Regulation

Ten-m protein is under the control of fushi tarazu and even-skipped, but not of opa (Baumgartner, 1994).

Targets of Activity

At least two pair-rule genes, paired and sloppy paired, and all segment-polarity genes analysed to date are under the control of Ten-m. Ten-m initiates a signal transduction cascade which acts either in concert with or via odd-paired, on downstream targets such as prd, slp and gooseberry, and through them, engrailed and wingless, leading to an opa-like phenotype (Baumgartner, 1994).

Protein Interactions

Ten-m is phosphorylated on tyrosine, resulting in an altered electrophoretic mobility. There are five putative tyrosine phosphorylation sites (Levine, 1994).


DEVELOPMENTAL BIOLOGY

Embryonic

The Ten-m protein is found in seven stripes during the blastoderm stage, each stripe overlapping the Even-skipped stripes (Baumgartner, 1994). Additional protein is seen in the lymph gland, cardiac cells, posterior spiracles and trachea. Expression is seen in the ventral nerve cord (CNS), the supraesophageal ganglia, and in hemocytes (Baumgartner, 1994).

Effects of Mutation or Deletion

Ten-m mutants show a phenotype resembling that of odd-paired, a member of the pair-rule class of segmentation genes (Baumgartner, 1994).


REFERENCES

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Tenascin major: Biological Overview | Evolutionary Homologs | Regulation | Developmental Biology | Effects of Mutation

date revised: 15 August 2008

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