Disease relevance of Lcp1

• In the ventral epidermis of Drosophila embryos, Wg specifies cells to secrete a characteristic pattern of denticles and naked cuticle that decorate the larval cuticle at the end of embryonic development [1].

High impact information on Lcp1

• Embryos that are homozygous mutant for both abl and dab fail to develop any axon bundles in the CNS, although the peripheral nervous system and the larval cuticle appear normal [2].
• Using the Ubx protein distribution as a marker for metameric organization and using Hoechst dye to monitor cell death, we could follow early events that lead to the final gap-segmentation phenotype in the larval cuticle [3].
• A 36 kilobase (kb) DNA segment of the Drosophila genome that contains several larval cuticle protein genes has been cloned and characterized [4].
• We have investigated the mechanistic aspects of inactivation of the major larval cuticle protein genes (Lcp1-4) in Drosophila miranda during Y chromosome evolution [5].
• DNA sequence analysis of the Y chromosomal Lcp gene locus reveals dense clustering of trapped retrotransposons [6].

Biological context of Lcp1

• The greatest difference between Lcp1 and Lcp2 is due to the occurrence of a pseudogene in D. melanogaster which is not present in D. miranda [7].
• Comparing the DNA sequences from D. miranda and D. melanogaster organization and the gene arrangement of Lcp1-Lcp4 are similar, although the intergene distances vary considerably [7].
• The larval cuticle protein genes (Lcps) represent a multigene family located at the right arm of the metacentric autosome 2 (2R) in Drosophila melanogaster [7].
• Evolution of the larval cuticle proteins coded by the secondary sex chromosome pair: X2 and neo-Y of Drosophila miranda: I. Comparison at the DNA sequence level [7].
• Regulation of larval cuticle protein gene expression in Drosophila melanogaster [8].

Anatomical context of Lcp1

• In larvae the cellular immune response involves circulating cells (hemocytes) that can be recruited from a hematopoietic organ located behind the brain, as well as a sessile population found just underneath the larval cuticle [9].
• Genetic analysis of both null and hypomorphic gbb alleles indicates that the gene is required in many developmental processes, including embryonic midgut morphogenesis, patterning of the larval cuticle, fat body morphology, and development and patterning of the imaginal discs [10].
• In a genetic screen for Tribolium mutants affecting the larval cuticle pattern, we isolated 4 mutants (from a total of 30) which disrupt segmentation in the thorax and abdomen [11].

Associations of Lcp1 with chemical compounds

• Two major larval cuticle proteins, LCP17 and LCP22, were purified from the guanidine hydrochloride extract of the larval cuticle, and specific antibodies were raised against these proteins [12].

Other interactions of Lcp1

• The Beagle element appears to inactivate the LCP-3 gene by inserting into its TATA box, but also may cause the precocious expression of two other LCP genes, LCP-1 and LCP-f2, in the cluster [8].
• Using the HUDSON, KREITMAN, and AGUADE (HKA) test, we show that the level of polymorphism in Lcp psi within D. melanogaster is lower than expected given the amount of divergence between D. melanogaster and D. simulans when the pseudogene data are compared to the Adh 5' flanking region [13].
• We show that zygotic mutations in several individual secretory pathway genes result in larval cuticle phenotypes nearly identical to those of CrebA mutants [14].
• The Drosophila Pax gene paired encodes a transcription factor that is required for the activation of segment-polarity genes and proper segmentation of the larval cuticle, postembryonic viability and male fertility [15].
• Antagonism between EGFR and Wingless signalling in the larval cuticle of Drosophila [16].

References