A Study of Maine Central Railroad Passenger Service Since 1900

A general study was made of the Maine Central railroad’s passenger service from 1900 to its elimination in I960. Because of the difficulties encountered in obtaining information regarding the Maine Central, the author has relied upon records of the Maine Public Utilities Commission and other sources. The Maine Central Railroad once operated an extensive network of passenger trains. Additional services also included airlines, buslines, ferries, and hotels. As the popularity of the automobile increased, the railroad was forced to curtail its passenger service and end all operations of ferries, buses, and hotels. The number of passengers steadily declined, and passenger deficits endangered the financial position of the railroad. Maine Central introduced articulated streamliners, reduced fares, and operated special trains to offset its losses. However, by 1954 officials began a major campaign to end all service. Several prominent Maine industries supported the railroad’s action in the hope of obtaining reduced freight rates. The last regularly scheduled passenger trains over Maine Central rails were operated on September 6, 1960. While the railroad was correct in arguing that the automobile and subsidized competition were responsible for passenger losses, Maine Central management was also to blame. Railroad buses directly competed with scheduled trains. After 1950 the quality of service rapidly declined, and little was done to promote passenger train travel. The passenger train problem is national, and the Maine Central presented a special problem because of its geographical location and lack of many industries along its routes to provide adequate freight revenues. Future students of Maine railroad history must take this into consideration in order to understand the railroad’s problem. While many questions regarding Maine Central’s passenger service remain unanswered, it is hoped this study may provide a foundation for further research

BIN1 Localizes the L-Type Calcium Channel to Cardiac T-Tubules

Cardiac tubular-like membrane invaginations contain the membrane scaffolding protein BIN1, which tethers dynamic microtubules that deliver calcium channels directly to T-tubule membrane

Abnormal Dosage Compensation of Reporter Genes Driven by the Drosophila Glass Multiple Reporter (GMR) Enhancer-Promoter

In Drosophila melanogaster the male specific lethal (MSL) complex is required for upregulation of expression of most X-linked genes in males, thereby achieving X chromosome dosage compensation. The MSL complex is highly enriched across most active X-linked genes with a bias towards the 3′ end. Previous studies have shown that gene transcription facilitates MSL complex binding but the type of promoter did not appear to be important. We have made the surprising observation that genes driven by the glass multiple reporter (GMR) enhancer-promoter are not dosage compensated at X-linked sites. The GMR promoter is active in all cells in, and posterior to, the morphogenetic furrow of the developing eye disc. Using phiC31 integrase-mediated targeted integration, we measured expression of lacZ reporter genes driven by either the GMR or armadillo (arm) promoters at each of three X-linked sites. At all sites, the arm-lacZ reporter gene was dosage compensated but GMR-lacZ was not. We have investigated why GMR-driven genes are not dosage compensated. Earlier or constitutive expression of GMR-lacZ did not affect the level of compensation. Neither did proximity to a strong MSL binding site. However, replacement of the hsp70 minimal promoter with a minimal promoter from the X-linked 6-Phosphogluconate dehydrogenase gene did restore partial dosage compensation. Similarly, insertion of binding sites for the GAGA and DREF factors upstream of the GMR promoter led to significantly higher lacZ expression in males than females. GAGA and DREF have been implicated to play a role in dosage compensation. We conclude that the gene promoter can affect MSL complex-mediated upregulation and dosage compensation. Further, it appears that the nature of the basal promoter and the presence of binding sites for specific factors influence the ability of a gene promoter to respond to the MSL complex