Evolution of histone gene loci in chironomid midges

Genome ◽  
1993 ◽  
Vol 36 (5) ◽  
pp. 852-862 ◽  
Author(s):  
Thomas Hankeln ◽  
Hans-Günther Keyl ◽  
Ralf Ross ◽  
Erwin R. Schmidt

In the present study we have localized the histone genes in the chromosomes of 16 different Chironomus species as well as in Prodiamesa olivacea, Glyptotendipes barbipes, and Acricotopus lucidus. In the genus of Chironomus we find four, five, or six different "major" chromosomal loci hybridizing with a histone gene cluster probe isolated from the genome of Chironomus thummi. These major histone gene loci probably contain clustered histone gene repeating units ("clustered" loci). They are located on one and the same chromosome arm in all but one of the species investigated. This shows that the histone gene clusters are rather conservative in their location over a long period of evolution. The comparison of the histone loci pattern from the chromosomes of the different chironomid species shows that there is good agreement with previously established chromosome maps and phylogenetic studies based on the chromosomal banding pattern. Stringent in situ hybridization with various histone gene containing clones suggest that the "clustered" histone gene loci are organized in a locus-specific way. In addition to the linked "clustered" histone gene loci, we found an isolated histone gene group ("orphon") present on chromosome IV in most Chironomus species. This gene group might be organized differently from the histone gene repeating unit described previously.Key words: histone genes, Chironomus, in situ hybridization, transposition, orphon.

Genomics ◽  
1994 ◽  
Vol 20 (2) ◽  
pp. 333-335 ◽  
Author(s):  
Nicholas Popescu ◽  
Drazen Zimonjic ◽  
Christopher Hatch ◽  
William Bonner

2007 ◽  
Vol 25 (18_suppl) ◽  
pp. 7570-7570 ◽  
Author(s):  
F. R. Hirsch ◽  
M. Varella-Garcia ◽  
P. A. Bunn ◽  
R. Dziadziuszko ◽  
Y. Xiao ◽  
...  

7570 Background: TRIBUTE was a phase III, placebo-controlled study of patients with previously untreated advanced NSCLC. Patients received erlotinib (E) (150 mg/d) or placebo, plus a course of 6 cycles of carboplatin and paclitaxel (CP), followed by maintenance E monotherapy (for those in the CP+E arm who were responding to treatment). 1,059 patients were randomized and treated (526 E; 533 placebo). There were no significant differences in OS, RR, or TTP between the two arms. In subgroup analyses of the pivotal 2nd line trial (BR21) of E in patients with relapsed NSCLC in which E significantly increased median survival (HR=0.71, p <0.0001), patients who scored positively for increased EGFR copy number by fluorescence in situ hybridization (FISH) exhibited prolonged OS (HR=0.44, p=0.008). Here we report on a similar subgroup analysis for TRIBUTE. Methods: FISH analysis was performed on all available tissue samples. FISH+ samples had a high level of polysomy (=four copies of the gene in =40% of cells), or gene amplification (presence of tight gene clusters, gene/chromosome per cell ratio =2, or =15 copies of the genes per cell in =10% of analyzed cells). Results: FISH analysis was successfully performed on 245 patients (121 E, 124 placebo). Outcome in the placebo patients from this subgroup was better than the overall population, suggesting that this subgroup may not be representative. Of the 100 patients (41%) that were FISH+, 33 had amplification and 67 had high polysomy. In FISH+ patients, OS was similar between those treated with CP+E and those treated with CP alone. However, FISH+ patients in the CP+E arm experienced a decrease in RR compared to those in the CP alone arm, and had a marginally significant longer TTP (HR=0.59, 0.35–0.99). The benefit in TTP appeared after approximately 6 months, during the maintenance portion of the trial. Conclusions: In this retrospective analysis, FISH+ did not predict survival benefit in TRIBUTE. A longer TTP, but a lower RR, was observed in the FISH+ patients. The lower RR in the CP+E arm in this group, taken together with the improved TTP during maintenance therapy, suggests that a non-concurrent combination approach (CP followed by E) warrants further investigation. No significant financial relationships to disclose.


Genome ◽  
2011 ◽  
Vol 54 (9) ◽  
pp. 771-778 ◽  
Author(s):  
Concepción Pérez-García ◽  
Paloma Morán ◽  
Juan J. Pasantes

The chromosomes of the invasive black-pigmy mussel (Xenostrobus securis (Lmk. 1819)) were analyzed by means of 4’,6-diamidino-2-phenylindole (DAPI) / propidium iodide (PI) and chromomycin A3 (CMA) / DAPI fluorescence staining and fluorescent in situ hybridization using major rDNA, 5S rDNA, core histone genes, linker histone genes, and telomeric sequences as probes. The diploid chromosome number in this species is 2n = 30. The karyotype is composed of seven metacentric, one meta/submetacentric, and seven submetacentric chromosome pairs. Telomeric sequences appear at both ends of every single chromosome. Major rDNA clusters appear near the centromeres on chromosome pairs 1 and 3 and are associated with bright CMA fluorescence and dull DAPI fluorescence. This species shows five 5S rDNA clusters close to the centromeres on four chromosome pairs (2, 5, 6, and 8). Three of the four core histone gene clusters map to centromeric positions on chromosome pairs 7, 10, and 13. The fourth core histone gene cluster occupies a terminal position on chromosome pair 8, also bearing a 5S rDNA cluster. The two linker histone gene clusters are close to the centromeres on chromosome pairs 12 and 14. Therefore, the use of these probes allows the unequivocal identification of 11 of the 15 chromosome pairs that compose the karyotype of X. securis.


The purpose of studies on the regulation of histone gene expression is to explain, for instance, how histone proteins arise in defined stoichiometric relationships in the chromatin, how transcription of histone genes is regulated in the cell cycle and how during the development of some species, histone variant genes are activated sequentially. The control of histone gene expression has m any interesting facets. One is struck by the major differences in balance and importance of the various regulatory mechanisms as they become apparent from investigations in m any laboratories. For example, in yeast, histone gene transcription is tightly coupled to the cell cycle, and the amounts of histone synthesized are determined largely by regulation of histone m RN A turnover (Hereford & Osley 1981). At the other extreme, there is the example of the maturing frog oöcyte where histone m RN A synthesis is uncoupled from DNA synthesis and yields pools of histone 1000-fold in excess of nuclear DNA mass (reviewed by Woodland 1980). Recent reports suggest that even the details of histone gene transcription may vary during the development of the species. The tandem histone gene clusters of sea urchin (G. Spinelli, unpublished results) and frog oocytes are transcribed polycistronically at least at some stages of their development (J. Gall, personal communication), whereas histone gene clusters of the cleaving sea urchin embryos appear to be transcribed monocistronically (Mauron et al. 1981). Finally, in the early embryo the partitioning of the m RN A between nucleus and cytoplasm may be also a regulative process (DeLeon al. 1983).


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