High impact information on TBR1

• We studied 68 MS patients and 39 normal controls with 1.5 T brain MRI [1].
• Expression of CAMKII-alpha and TBR1 mRNAs was significantly increased in bipolar patients but not in major depressed patients, and there was a trend toward reduced BDNF expression in both groups [2].
• CONCLUSIONS: The findings that TBR1 and CAMKII-alpha expression is increased only in bipolar patients suggests abnormalities of specific genes related to a major cortical cell type and its connectivity [2].
• We also noted that the P. flava homolog of T-brain/Eomes, a gene closely related by sequence and expression around the blastopore to Brachyury and associated with development of the vertebrate brain, also exhibits early posterior expression around the blastopore and a field of de novo anterior ectoderm expression during later embryogenesis [3].
• T-Brain expression in the apical organ of hemichordate tornaria larvae suggests its evolutionary link to the vertebrate forebrain [4].

Anatomical context of TBR1

• Although most of the T-box genes are involved in the mesoderm formation of chordate embryos, mammalian T-Brain is expressed in the developing central nervous system, and defines molecularly distinct domains within the cerebral cortex [4].

Other interactions of TBR1

• The copy number gains of CDKN1C and INS and the copy number losses of TBR1 were significantly correlated with longer survival of patients [5].
• The gene regulatory mechanisms responsible for initiating the anterior zone of de novo expression of T-brain may represent a cooption to specify early neuroectoderm of the regulatory program evolved first to drive anterior Brachyury expression for deuterostome mouth formation [3].

References