High impact information on Ipw

• The data suggest the presence of a paternally expressed structural gene between Snrpn and Ipw whose deficiency causes lethality, although other possibilities exist, including position effects on expression of imprinted genes or that simultaneous deficiency of both ORFs of Snrpn causes lethality [1].
• We have now cloned a mouse gene, named Ipw, that has sequence similarity to a part of IPW and is located in the conserved homologous region of mouse chromosome 7 [2].
• The Ipw cDNA also contains no long open reading frame, is alternatively spliced and contains multiple copies of a 147 bp repeat, arranged in a head-to-tail orientation, that are interrupted by the insertion of an intracisternal A particle sequence [2].
• Although Snrpn, Ipw and MBII-85 are putatively transcribed from the same promoter, the transcripts are differentially detected in neural tissues [3].
• We have physically mapped the 1-Mb critical region, which lies between the Gabrb3 and Ube3a/Ipw genes, and DNA sequencing has localized a new member of the third subfamily of P-type ATPases to the minimal region specifying the trait [4].

Biological context of Ipw

• The unusual inheritance pattern of this phenotype suggests either genomic imprinting, known to occur in other local genes (Ube3a, Ipw), or an effect of maternal haploinsufficiency during pregnancy or lactation on body fat in the progeny [4].

References