PARENT SESSION
1:30 PM to 3:30 PM
Monday, April 22, 2002
Poster Session 10 Cell Cycle Effects
Room: Nevada Exhibition Center

(P15-147) Identification and characterization of novel human HRAD9 and mouse Mrad9 paralogues.

Hopkins, Kevin^*,1, Wang, Xiaojian¹, Morales, Ayana¹, Hang, Haiying¹, Lieberman, Howard¹, ¹ Center for Radiological Research, New York, NY

ABSTRACT-
The HRAD9 and Mrad9 genes mediate radioresistance and regulate the G2/M cell cycle checkpoint induced by ionizing radiation. Consequently, a targeted deletion within Mrad9 causes mouse embryonic stem cells to be radiosensitive and unable to transiently delay cycling in response to radiation exposure. Screening of the public human genomic DNA sequence database and the mouse EST database for HRAD9 and Mrad9 like genes led to the identification of related DNA sequences in both databases that encoded part of an ORF. Based on these incomplete DNA sequences, cDNAs comprising full-length ORFs and 3' untranslated regions have been isolated. The ORF of the human orthologue (called HRAD9B) is 1.242kb and encodes a protein that is 414 amino acids long. The ORF of the mouse gene (called Mrad9B) is 1.212kb and can encode a protein that is 404 amino acids in length. These two proteins have 35% amino acid identity with their respective, related human and mouse protein paralogues. Studies are underway to determine if these alternative forms of HRAD9 and Mrad9 are involved in cell cycle checkpoint control and the promotion of resistance to ionizing radiation, UV light and other agents capable of damaging DNA. Furthermore, the possibility that the functions of these genes might be redundant is also being tested.

KEYWORDS: hrad9, mrad9, paralogues