Disease relevance of Twist2

• Mice homozygous for a twist-2 null allele or doubly heterozygous for twist-1 and -2 alleles show elevated expression of proinflammatory cytokines, resulting in perinatal death from cachexia [1].

High impact information on Twist2

• Dorsally, they accumulate under the ectoderm and express a non-muscle dermal marker, Dermo-1 [2].
• Homologous introduction of cre recombinase into the Dermo1 (Twist2) gene locus resulted in robust expression of CRE in mesenchymal condensations giving rise to both osteoblast and chondrocyte lineages [3].
• Msx1 expression was investigated in the context of the onset of dermis formation monitored by the Dermo1 gene expression [4].
• Conversely, when beta-catenin was activated in En1 cells, it induces Dermo1 expression in all cells of the En1 domain and disrupts muscle gene expression [5].
• These analyses demonstrated that Dermo-1 mRNA was expressed in these osteoblast-like cell lines [6].

Biological context of Twist2

• To confirm Dermo-1 mRNA expression in osteoblastic cells, we performed reverse transcription polymerase chain reaction (RT-PCR) analysis using mRNA from ROS17/2.8 cells and MC3T3-E1 cells by Dermo-1 specific primers and Northern blot analysis [6].

Analytical, diagnostic and therapeutic context of Twist2

• When the essential Wnt transducer beta-catenin is mutated in En1 cells, it results in the loss of Dermo1-expressing dorsal dermal progenitors and dermis [5].
• Using the RT-PCR method, the mRNA levels of Dermo-1 and twist were found to be decreased by the treatment with rhBMP-2 in C3H10T1/2 cells [6].
• We also observed that the mRNA level of Dermo-1 was decreased about fourfold by the treatment with rhBMP-2 in C3H10T1/2 cells by Northern blot analysis [6].

References