Genome-wide studies have identified thousands of long noncoding RNAs (lncRNAs) 
lacking protein-coding capacity. However, most lncRNAs are expressed at a very 
low level, and in most cases there is no genetic evidence to support their in 
vivo function. Malat1 (metastasis associated lung adenocarcinoma transcript 1) 
is among the most abundant and highly conserved lncRNAs, and it exhibits an 
uncommon 3'-end processing mechanism. In addition, its specific nuclear 
localization, developmental regulation, and dysregulation in cancer are 
suggestive of it having a critical biological function. We have characterized a 
Malat1 loss-of-function genetic model that indicates that Malat1 is not 
essential for mouse pre- and postnatal development. Furthermore, depletion of 
Malat1 does not affect global gene expression, splicing factor level and 
phosphorylation status, or alternative pre-mRNA splicing. However, among a small 
number of genes that were dysregulated in adult Malat1 knockout mice, many were 
Malat1 neighboring genes, thus indicating a potential cis-regulatory role of 
Malat1 gene transcription.