Juvenile hormone acid O-methyltransferase in Drosophila melanogaster

Juvenile hormone (JH) acid O-methyltransferase (JHAMT) is the enzyme that transfers a methyl groupfrom S-adenosyl-L-methionine (SAM) to the carboxyl group of JH acids to produce active JHs in thecorpora allata. While the JHAMT gene was originally identified and characterized in the silkwormBombyx mori, no orthologs from other insects have been studied until now. Here we report on thefunctional characterization of the CG17330/DmJHAMT gene in the fruit fly Drosophila melanogaster.Recombinant DmJHAMT protein expressed in Escherichia coli catalyzes the conversion of farnesoic acidand JH III acid to their cognate methyl esters in the presence of SAM. DmJHAMT is predominantlyexpressed in corpora allata, and its developmental expression profile correlates with changes in the JHtiter. While a transgenic RNA interference against DmJHAMT has no visible effect, overexpression ofDmJHAMT results in a pharate adult lethal phenotype, similar to that obtained with application of JHanalogs, suggesting that the temporal regulation of DmJHAMT is critical for Drosophila development

Pituitary Apoplexy Producing Internal Carotid Artery Compression: A Case Report

We report a case of pituitary apoplexy resulting in right internal carotid artery occlusion accompanied by hemiplegia and lethargy. A 43-yr-old man presented with a sudden onset of severe headache, visual disturbance and left hemiplegia. Investigations revealed a nodular mass, located in the sella and suprasellar portion and accompanied by compression of the optic chiasm. The mass compressed the bilateral cavernous sinuses, resulting in the obliteration of the cavernous portion of the right internal carotid artery. A border zone infarct in the right fronto-parietal region was found. Transsphenoidal tumor decompression following conservative therapy with fluid replacement and steroids was performed. Pathological examination revealed an almost completely infarcted pituitary adenoma. The patient's vision improved immediately after the decompression, and the motor weakness improved to grade IV+ within six months after the operation. Pituitary apoplexy resulting in internal carotid artery occlusion is rare. However, clinicians should be aware of the possibility and the appropriate management of such an occurrence

Precocious Metamorphosis in the Juvenile Hormone–Deficient Mutant of the Silkworm, Bombyx mori

Insect molting and metamorphosis are intricately governed by two hormones, ecdysteroids and juvenile hormones (JHs). JHs prevent precocious metamorphosis and allow the larva to undergo multiple rounds of molting until it attains the proper size for metamorphosis. In the silkworm, Bombyx mori, several “moltinism” mutations have been identified that exhibit variations in the number of larval molts; however, none of them have been characterized molecularly. Here we report the identification and characterization of the gene responsible for the dimolting (mod) mutant that undergoes precocious metamorphosis with fewer larval–larval molts. We show that the mod mutation results in complete loss of JHs in the larval hemolymph and that the mutant phenotype can be rescued by topical application of a JH analog. We performed positional cloning of mod and found a null mutation in the cytochrome P450 gene CYP15C1 in the mod allele. We also demonstrated that CYP15C1 is specifically expressed in the corpus allatum, an endocrine organ that synthesizes and secretes JHs. Furthermore, a biochemical experiment showed that CYP15C1 epoxidizes farnesoic acid to JH acid in a highly stereospecific manner. Precocious metamorphosis of mod larvae was rescued when the wild-type allele of CYP15C1 was expressed in transgenic mod larvae using the GAL4/UAS system. Our data therefore reveal that CYP15C1 is the gene responsible for the mod mutation and is essential for JH biosynthesis. Remarkably, precocious larval–pupal transition in mod larvae does not occur in the first or second instar, suggesting that authentic epoxidized JHs are not essential in very young larvae of B. mori. Our identification of a JH–deficient mutant in this model insect will lead to a greater understanding of the molecular basis of the hormonal control of development and metamorphosis