Abstract :
Homo sapiens C/D box snoRNA U14A. This snoRNA was originally cloned in the mouse by Maxwell and Martin (1986) and named "4.5S hybridizing RNA" or hybRNA, due to its capability to hybridize with 18S rRNA in vitro. Trinh-Rohlik and Maxwell (1988) and Li et al. (1990) recognized two domains of conserved complementarity between U14 and 18S rRNA. Li et al. (1990) found that the deletion of U14 (snR128) disrupts the production of 18S rRNA in the yeast S. cerevisiae, while Liang and Fournier (1995) showed that compensatory mutations in U14 domain A and 18S rRNA could restore 18S rRNA processing. In yeast, multiple base substitutions in domain A, but not domain B, are lethal (Jarmolowski et al., 1990). The two domains are however functionally interdependent, as points mutations in domain A that don't affect growth are lethal when combined with the disruption of base-pairing at the level of domain B (Liang and Fournier, 1995). U14 is also required for the processing of a pre-rRNA substrate in mouse extracts, although the substrate lacked the 18S element complementary to U14 domain B (Enright et al., 1996).
Leverette et al. (1992) showed that mouse U14 snRNA is processed from introns of the hsc70 (heat shock cognate protein ) pre-mRNA. U14 was postulated to guide the 2'O-ribose methylation of 18S rRNA C462 at the level of domain B by Kiss-Laszlo et al. (1996). Base-pairing at the level of domain A could function as a chaperone in the processing of 18S rRNA. The human snoRNA U14A, and a closely related copy, U14B, reside in introns of the RPS13 gene.
GenBank accession number :
Host gene : RPS13 (ribosomal protein S13)
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Target RNA : 18S rRNA C462
sno/scaRNAs with same target 18S rRNA C462 :U14B