Ribosomal DNA organization before and after magnification in Drosophila melanogaster.

In all eukaryotes, the ribosomal RNA genes are stably inherited redundant elements. In Drosophila melanogaster, the presence of a Ybb(-) chromosome in males, or the maternal presence of the Ribosomal exchange (Rex) element, induces magnification: a heritable increase of rDNA copy number. To date, several alternative classes of mechanisms have been proposed for magnification: in situ replication or extra-chromosomal replication, either of which might act on short or extended strings of rDNA units, or unequal sister chromatid exchange. To eliminate some of these hypotheses, none of which has been clearly proven, we examined molecular-variant composition and compared genetic maps of the rDNA in the bb(2) mutant and in some magnified bb(+) alleles. The genetic markers used are molecular-length variants of IGS sequences and of R1 and R2 mobile elements present in many 28S sequences. Direct comparison of PCR products does not reveal any particularly intensified electrophoretic bands in magnified alleles compared to the nonmagnified bb(2) allele. Hence, the increase of rDNA copy number is diluted among multiple variants. We can therefore reject mechanisms of magnification based on multiple rounds of replication of short strings. Moreover, we find no changes of marker order when pre- and postmagnification maps are compared. Thus, we can further restrict the possible mechanisms to two: replication in situ of an extended string of rDNA units or unequal exchange between sister chromatids.

Benign splenosis mimicking peritoneal seeding in a bladder cancer patient: a case report.

INTRODUCTION: Splenosis is a post-traumatic autotrasplantation and proliferation of splenic tissue in ectopic sites. These implants may mimic malignancy in healthy patients or peritoneal metastases in cancer patients. When a previous history of splenic injury is known, the finding of soft tissue nodules in many thoracic and abdominal locations might raise the suspicion of the benign condition of splenosis, in order to avoid unnecessary surgery or chemotherapy. CASE PRESENTATION: A 56-year-old man with history of persistent hematuria from bladder cancer was referred to our Institution for suspected peritoneal carcinosis. For staging purposes he underwent abdominal computed tomography and ultrasound. The integration of patient's history and imaging results led to the diagnosis of peritoneal splenosis. The patient therefore underwent regular Trans Urethral Resection of Bladder for the known malignancy; while no treatment was necessary for splenosis. Two years follow-up was negative for metastases. CONCLUSION: Splenosis is a benign condition after traumatic splenectomy which should be taken into account in the differential diagnosis with peritoneal seeding of malignancy because its appearance may resemble malignancy.

Genetic evidence that nonhomologous disjunction and meiotic drive are properties of wild-type Drosophila melanogaster male meiosis.

We have followed sex and second chromosome disjunction, and the effects of these chromosomes on sperm function, in four genotypes: wild-type males, males deficient for the Y-linked crystal locus, males with an X chromosome heterochromatic deficiency that deletes all X-Y pairing sites, and males with both deficiencies. Both mutant situations provoke chromosome misbehavior, but the disjunctional defects are quite different. Deficiency of the X heterochromatin, consonant with the lack of pairing sites, mostly disrupts X-Y disjunction with a decidedly second-level effect on major autosome behavior. Deleting crystal, consonant with the cytological picture of postpairing chromatin-condensation problems, disrupts sex and autosome disjunction equally. Even when the mutant-induced nondisjunction has very different mechanics, however, and even more importantly, even in the wild type, there is strong, and similar, meiotic drive. The presence of meiotic drive when disjunction is disrupted by distinctly different mechanisms supports the notion that drive is a normal cellular response to meiotic problems rather than a direct effect of particular mutants. Most surprisingly, in both wild-type and crystal-deficient males the Y chromosome moves to the opposite pole from a pair of nondisjoined second chromosomes nearly 100% of the time. This nonhomologous interaction is, however, absent when the X heterochromatin is deleted. The nonhomologous disjunction of the sex and second chromosomes may be the genetic consequence of the chromosomal compartmentalization seen by deconvolution microscopy, and the absence of Y-2 disjunction when the X heterochromatin is deleted suggests that XY pairing itself, or a previously unrecognized heterochromatic function, is prerequisite to this macrostructural organization of the chromosomes.

Does Stellate cause meiotic drive in Drosophila melanogaster?

Drosophila melanogaster males deficient for the crystal (cry) locus of the Y chromosome that carry between 15 and 60 copies of the X-linked Stellate (Ste) gene are semisterile, have elevated levels of nondisjunction, produce distorted sperm genotype ratios (meiotic drive), and evince hyperactive transcription of Ste in the testes. Ste seems to be the active element in this system, and it has been proposed that the ancestral Ste gene was "selfish" and increased in frequency because it caused meiotic drive. This hypothetical evolutionary history is based on the idea that Ste overexpression, and not the lack of cry, causes the meiotic drive of cry(-) males. To test whether this is true, we have constructed a Ste-deleted X chromosome and examined the phenotype of Ste(-)/cry(-) males. If hyperactivity of Ste were necessary for the transmission defects seen in cry(-) males, cry(-) males completely deficient for Ste would be normal. Although it is impossible to construct a completely Ste(-) genotype, we find that Ste(-)/cry(-) males have exactly the same phenotype as Ste(+)/cry(-) males. The deletion of all X chromosome Ste copies not only does not eliminate meiotic drive and nondisjunction, but it also does not even reduce them below the levels produced when the X carries 15 copies of Ste.

Endoscopic ultrasound and Computed Tomography in gastric stromal tumours.

PURPOSE: Gastric stromal tumors (GIST) have no well defined biological characteristics, from either the pathological or immunohistochemical point of view, which can make their definition by imaging techniques difficult. We evaluated CT and EUS morphologic characteristics and signs of malignancy of eleven cases of GIST and compared the findings to the pathological classification. MATERIAL AND METHODS: EUS was performed with a 100 degrees, 5-7.5 MHz convex probe on a Pentax endoscope and CT using the byphasic spiral technique. RESULTS: The 11 GIST cases were ranked according to the criteria of malignancy defined by each of the two imaging techniques. There was a close correlation between the imaging-based and pathological classifications. CONCLUSIONS: Size and homogeneous pattern prove to be the most reliable criteria to differentiate between benign and malignant lesions. EUS is more accurate than CT in diagnosing the nature of GIST, but CT allows a more complete and comprehensive evaluation. The data provided by the imaging techniques are fundamental to plan the therapeutic approach.