We used RNA-Seq analysis of embryonic mRNAs and show that loss of Praeruptorin-B heph03429 function results in misregulation of numerous transcripts, including those known to be functionally involved in dorso-ventral patterning and dorsal closure during embryogenesis. Some of these mechanisms may be similar to how the mammalian PTB regulates aspects of mRNA processing. We note that identification of Albaspidin-AA downstream targets by searching for potential binding sites alone is challenging because PTB binds short, degenerate sequences UCUU and UUCUthat are found frequently throughout the genome. In the future, a crosslinking/immunoprecipitation experiment that detects RNA-protein interactions on a genome-wide levelneeds to be combined with our high throughput sequencing dataset to identify the subset of candidates that directly bind dmPTB. In summary, our combined results indicate that dmPTB acts as a potent upstream regulator that specifically controls several downstream target genes and processes during embryogenesis. Many genes or transcripts altered in the heph03429 mutanthave known functional connections to specific cellular and developmental processes during embryonic development, such as neurogenesis, dorso-ventral axis formation, and dorsal closure. For others, such as down-regulation of cuticular proteins and mRNA processing defects, functional relevance is not obvious at this stage. Genes identified in this study provide entry points and new avenues for future studies on mechanisms and biological functions as to how an RNA-binding protein controls gene expression and embryonic development. The efficacy of cisplatin is limited, however, by severe side effects such as nephrotoxicity, neurotoxicity, ototoxicity, and emetogenicity. In particular, the nephrotoxicity of cisplatin is dose dependent and therefore limits the amount of drug that can be administered. Procedures to reduce such toxicity include aggressive hydration with saline and simultaneous administration of mannitol, which is now accepted as the standard of care for individuals treated with regimens containing a high doseof cisplatin. Unfortunately, renal toxicity still occurs even with such hydration, highlighting the need for more effective preventive strategies. Another approach to limiting the nephrotoxicity of cisplatin is intravenous magnesium supplementation. Cisplatin-induced nephrotoxicity is accompanied by disturbance of the renal handling of electrolytes. In particular, depletion of magnesium has emerged as a common event associated with the acute renal toxicity induced by the drug. Whereas several studies have demonstrated the efficacy of magnesium supplementation for prevention of hypomagnesemia during cisplatin treatment, only two prospective studies, each featuring a relatively small number of patients, have evaluated its efficacy in terms of protection against cisplatininduced nephrotoxicity. Despite the dearth of evidence in support of a beneficial effect of magnesium supplementation therapy on the renal toxicity of cisplatin, intravenous administration of magnesium is currently recommended for outpatients receiving high-dose cisplatin with a short hydration regimen. We have therefore recently applied this procedure to all patients who receive such chemotherapy. However, given that magnesium supplementation has not been accepted as the standard of care, at least in Japan, most patients who receive high-dose cisplatin are treated.