Malat1 is an abundant long, noncoding RNA that localizes to nuclear bodies known 
as nuclear speckles, which contain a distinct set of pre-mRNA processing 
factors. Previous studies in cell culture have demonstrated that Malat1 
interacts with pre-mRNA splicing factors, including the serine- and 
arginine-rich (SR) family of proteins, and regulates a variety of biological 
processes, including cancer cell migration, synapse formation, cell cycle 
progression, and responses to serum stimulation. To address the physiological 
function of Malat1 in a living organism, we generated Malat1-knockout (KO) mice 
using homologous recombination. Unexpectedly, the Malat1-KO mice were viable and 
fertile, showing no apparent phenotypes. Nuclear speckle markers were also 
correctly localized in cells that lacked Malat1. However, the cellular levels of 
another long, noncoding RNA--Neat1--which is an architectural component of 
nuclear bodies known as paraspeckles, were down-regulated in a particular set of 
tissues and cells lacking Malat1. We propose that Malat1 is not essential in 
living mice maintained under normal laboratory conditions and that its function 
becomes apparent only in specific cell types and under particular conditions.