Expression data from 6 day-old Atxn1L-/- and Atxn1-/- lung tissues

Although expansion of a polyglutamine tract in ATAXIN1 (ATXN1) causes Spinocerebellar ataxia type 1, the functions of wild-type ATXN1 and ATAXIN1-Like (ATXN1L) remain poorly understood. To gain insight into the function of these proteins, we generated and characterized Atxn1L-/- and Atxn1-/- ; Atxn1L-/- double mutant animals. We found that Atxn1L -/- mice have several developmental problems including hydrocephalus, omphalocoele and lung alveolarization defects. These phenotypes are more penetrant and severe in Atxn1-/- ; Atxn1L-/- mice, suggesting that Atxn1 and Atxn1L are functionally redundant. To unravel the molecular mechanism underlying the alveolarization defect in Atxn1-/- mice, we carried out microarray analyses using total lung RNA from WT, Atxn1-/- and Atxn1L-/- mice Lung tissues were dissected from 6 day old mice from either Atxn1 heterozyous intercrosses or Atxn1L heterozygous intercrosses. We collected lung tissue samples from 4 pairs of WT and Atxn1-/- amd 3 pairs of WT and Atxn1-/- mice. Total RNA extracted from the samples was subjected to microarray analysis using Affymetrix mouse gene ST 1.0 array. GSM731591-GSM731598 (Atxn1L KO and controls) and GSM731599-GSM731604 (Atxn1 KO and controls) were RMA-processed separately.