The apterous gene mutations is a recessive trait that is inherited causing a varying phenotypes such as different wing deformities. Other phenotypes observed are the decrease in life span and female sterility. Ap is required to regulate gene expression needed for the development of Drosophila wings and haltere discs. Decreased ap activity due to the overexpression of dLMO results in wing mutations. The phenotypes displayed in apterous mutants are places them at a disadvantage compared to wild type flies.
Introduction Drosophila melanogaster with apterous mutations usually lack fully functional wings. There are many distinct phenotypes expressed with this mutation. The mutants usually lack wing blades but other abnormalities could be expressed …show more content…
The ap gene is a new member of the LIM family of developmental regulatory proteins that is characterized by the presence of LIM domain and homeo domain. The ap protein shows an amino acid sequence similar to the lin-11 and mec-3 proteins of Caenorhabditis elegans. Ap function is required for normal wing and haltere disc development in fruit flies during the third larval instar. The mutations in recessive flies are consistent with ap expression patterns in the larval imaginal discs. Ap regulates the expressions of genes that are needed for the growth and pattern formation of Drosophila melanogaster wings and haltere discs. In ap mutants, the haltere discs and wing size are reduced and those that are wingless the ap are associated with extensive cell death in the wing blade region of the wing discs. There are several genes that mutations have caused wing and haltere structure deformities other than ap such as mutations in the vg …show more content…
LIM domains mediate protein-protein interactions and block DNA binding activity of the homeodomain. dLDB is the protein that is the cofactor for LIM-homeodomain binding to the LIM domains. During wing development, ap regulates its own activity by inducing the expression of the Beadex/dLMO gene. This gene encodes a LIM domain containing protein called dLMO. dLMO has sequences similar to the LIM domains of ap and compete with ap to bind with dLDB therefore inactivating ap. When apterous induces expression of Serrate and Fringe genes, it represses the Delta. Ap also subsequently induces expression of dLMO which then reduces ap activity levels that allows the expression of Delta and leads to the down regulation of Serrate and Fringe. The overexpression of Serrate and reduced expression of Delta when there is a loss of dLMO leads to the defects in wing development. The phenotypes showing wing deformities are due to the excess of ap activity so dLMO serves as a regulator of the ap activity during the development of Drosophila wings. Experiments were done showing that dLMO inhibits ap activity by competing effectively for ap activity but it is not the same vice versa. When dLAP, a fushion protein with LIM domains of dLMO and ap sequences, was introduced to a mutant cell with reduced ap activity, it was able to increase ap activity levels
Introduction Drosophila melanogaster with apterous mutations usually lack fully functional wings. There are many distinct phenotypes expressed with this mutation. The mutants usually lack wing blades but other abnormalities could be expressed …show more content…
The ap gene is a new member of the LIM family of developmental regulatory proteins that is characterized by the presence of LIM domain and homeo domain. The ap protein shows an amino acid sequence similar to the lin-11 and mec-3 proteins of Caenorhabditis elegans. Ap function is required for normal wing and haltere disc development in fruit flies during the third larval instar. The mutations in recessive flies are consistent with ap expression patterns in the larval imaginal discs. Ap regulates the expressions of genes that are needed for the growth and pattern formation of Drosophila melanogaster wings and haltere discs. In ap mutants, the haltere discs and wing size are reduced and those that are wingless the ap are associated with extensive cell death in the wing blade region of the wing discs. There are several genes that mutations have caused wing and haltere structure deformities other than ap such as mutations in the vg …show more content…
LIM domains mediate protein-protein interactions and block DNA binding activity of the homeodomain. dLDB is the protein that is the cofactor for LIM-homeodomain binding to the LIM domains. During wing development, ap regulates its own activity by inducing the expression of the Beadex/dLMO gene. This gene encodes a LIM domain containing protein called dLMO. dLMO has sequences similar to the LIM domains of ap and compete with ap to bind with dLDB therefore inactivating ap. When apterous induces expression of Serrate and Fringe genes, it represses the Delta. Ap also subsequently induces expression of dLMO which then reduces ap activity levels that allows the expression of Delta and leads to the down regulation of Serrate and Fringe. The overexpression of Serrate and reduced expression of Delta when there is a loss of dLMO leads to the defects in wing development. The phenotypes showing wing deformities are due to the excess of ap activity so dLMO serves as a regulator of the ap activity during the development of Drosophila wings. Experiments were done showing that dLMO inhibits ap activity by competing effectively for ap activity but it is not the same vice versa. When dLAP, a fushion protein with LIM domains of dLMO and ap sequences, was introduced to a mutant cell with reduced ap activity, it was able to increase ap activity levels