Disease relevance of up

• All retroviruses and retrotransposons studied to date regulate the relative levels of gag and pol/int gene products post-transcriptionally from a single mRNA [1].
• Sp3 inhibits Sp1-mediated activation of the cardiac troponin T promoter and is downregulated during pathological cardiac hypertrophy in vivo [2].

High impact information on up

• Characterization of these new Mhc alleles suggests that hypercontraction occurs via a mechanism, which is molecularly distinct from mutants identified previously in troponin I and troponin T [3].
• ACE splicing activity was competed by RNAs containing the purine-rich splicing enhancer from cardiac troponin T exon 5 [4].
• This mechanism is not exclusive to the Troponin T gene, but is also relevant to the muscle-specific Troponin I gene [5].
• The S185F substitution in Tm2 is close to a troponin T binding site on tropomyosin [6].
• Differential muscle-type expression of the Drosophila troponin T gene. A 3-base pair microexon is involved in visceral and adult hypodermic muscle specification [7].

Biological context of up

• We determined the nucleotide sequences of troponin-T genes in five extant mutants [8].
• In situ hybridization of the Drosophila troponin-T gene to polytene chromosomes demonstrated that it resides within subdivision 12A of the X chromosome, precisely where upheld and indented thorax flight muscle mutations have been mapped previously [8].
• Two of the alleles, upheld2 and upheld3, apparently disrupt RNA splicing and eliminate most or all troponin-T from flight and jump muscles, while the remaining three alleles change the identities of single amino acids of troponin-T [8].
• This decrease in expression levels of the distinct thin-filament components led us to postulate that any change in the amount of TnT transcripts might trigger the down-regulation of other co-regulated thin-filament components [9].
• Two functionally identical modular enhancers in Drosophila troponin T gene establish the correct protein levels in different muscle types [5].

Anatomical context of up

• All flies that overexpress TnT were unable to fly, and the loss of thin filaments themselves was coupled with ultrastructural perturbations of the sarcomere [9].
• Immunolabeling for TnT in all these muscle cells appeared in moderate amounts at any point along the sarcomere length, except for the central zone of the A band (H band) [10].
• Akazara scallop troponin T contains 55 amino acid residues more and 82 residues fewer than rabbit skeletal muscle troponin T and Drosophila melanogaster troponin T, respectively, showing almost the lowest sequence homology with rabbit troponin T (26%) but the highest homology with Drosophila troponin T (33%) [11].
• We show by the use of gene fusion constructs that the subgenomic 2 kilobase copia RNA, encoding gag products, is expressed as protein in cultured cells at least ten-fold more efficiently than the full genome length RNA, which additionally contains the pol and int open reading frames [1].
• (i) Placode formation and the expression of wingless-int (Wnt) 7a and Msx-1 in the placode epithelium are mesenchyme dependent [12].

Other interactions of up

• However, in a Sh mutant background, ine mutations cause downturned wings and an indented thorax [13].

Analytical, diagnostic and therapeutic context of up

• They have been identified as isoforms of troponin-T (TnT) by sequence analysis of a cDNA clone isolated from an embryonic library [14].

References