Cyclin T2A Gene Maps on Human Chromosome 2q21

Abstract

Cyclin T2a was recently identified as one of the regulatory subunits of the cdk–cyclin complex P-TEFb, the most studied positive factor in the regulation of transcription elongation. By fluorescent in situ hybridization (FISH), the gene codifying for cyclin T2a has been mapped on human chromosome 2q21. This locus also has been linked to different forms of myopathy. By use of a new specific antiserum raised against cyclin T2a, the immunohistochemical pattern of expression of cyclin T2a in human tissues has been examined and compared to that of cyclin T1, described in the previous report. The observation that immunohistochemical expression of cyclin T2a was high in skeletal muscle cells, whereas it was undetectable in two cases of centronuclear myopathy, together with its chromosomal location, suggests an involvement of the cdk9–cyclin T2a complex in this disease.

Cyclin T: Three forms for different roles in physiological and pathological functions

“…This expression pattern is very similar to that described above for cyclin T1 (De Luca et al, 2001b) and in agreement with mRNA distribution for cyclin T2a (Peng et al, 1998b).…”

“…A different tissue distribution and/or level of expression is detected in several organs. To note, tissues of mesenchymal origin, such as connective tissue, skeletal muscle, and myocardial cells, adipocytes, chondrocytes, and endothelial cells, as well as blood and lymphoid tissues, exhibits high cyclin T1 expression levels (De Luca et al, 2001b).…”

“…Effectively, the activity of CDK9/cyclin T complex is increased in this system, suggesting a role in muscle differentiation. Moreover, cyclin T2a protein level is high in human adult skeletal muscle cells (De Luca et al, 2001b). The high immunohistochemical expression level of cyclin T2a in adult muscle cells, as well as the peak of expression reached during in vitro muscle differentiation, suggests that CDK9/cyclin T2a complex might promote myogenic differentiation eliciting the expression of muscle-specific genes (De Luca et al, 2001b).…”

“…Moreover, cyclin T2a protein level is high in human adult skeletal muscle cells (De Luca et al, 2001b). The high immunohistochemical expression level of cyclin T2a in adult muscle cells, as well as the peak of expression reached during in vitro muscle differentiation, suggests that CDK9/cyclin T2a complex might promote myogenic differentiation eliciting the expression of muscle-specific genes (De Luca et al, 2001b). Human cyclin T2a gene maps on chromosome locus 2q21 (De Luca et al, 2001b), a locus involved in different forms of autosomal dominant myopathies Pelin et al, 1999;Xiang et al, 1999).…”

“…The high immunohistochemical expression level of cyclin T2a in adult muscle cells, as well as the peak of expression reached during in vitro muscle differentiation, suggests that CDK9/cyclin T2a complex might promote myogenic differentiation eliciting the expression of muscle-specific genes (De Luca et al, 2001b). Human cyclin T2a gene maps on chromosome locus 2q21 (De Luca et al, 2001b), a locus involved in different forms of autosomal dominant myopathies Pelin et al, 1999;Xiang et al, 1999). Myopathies are non-inflammatory primary degenerative muscle diseases that become symptomatic in infancy or childhood and are characterized by proximal or diffuse muscle weakness (Pearson et al, 1967).…”