Poly(dC?dA/dG?dT) repeats in the Drosophila genome: a key function for dosage compensation and position effects?

Chromosoma ◽  
1987 ◽  
Vol 95 (3) ◽  
pp. 209-215 ◽  
Author(s):  
Peter Huijser ◽  
Wolfgang Hennig ◽  
Rosilde Dijkhof
Cell ◽  
1984 ◽  
Vol 36 (2) ◽  
pp. 469-481 ◽  
Author(s):  
Tulle Hazelrigg ◽  
Robert Levis ◽  
Gerald M. Rubin

Development ◽  
1995 ◽  
Vol 121 (11) ◽  
pp. 3573-3582 ◽  
Author(s):  
R.R. Roseman ◽  
J.M. Swan ◽  
P.K. Geyer

The suppressor of Hairy-wing [su(Hw)] gene encodes a zinc finger protein that binds to a repeated motif in the gypsy retrotransposon. These DNA sequences, called the su(Hw)-binding region, have properties of an insulator region because they (1) disrupt enhancer/silencer function in a position-dependent manner and (2) protect the mini-white gene from both euchromatic and heterochromatic position effects. To gain further insights into the types of position effects that can be insulated, we determined the effects of the su(Hw)-binding region on dosage compensation of the X-linked mini-white gene. Dosage compensation is the process that equalizes the unequal content of X-linked genes in males and females by increasing the X-linked transcription level twofold in males. Transposition of X-linked genes to the autosomes commonly results in incomplete dosage compensation, indicating that the distinct male X chromatin environment is important for this process. We found that dosage compensation of autosomally integrated mini-white genes flanked by su(Hw)-binding regions was greatly improved, such that complete or nearly complete compensation was observed at the majority of insertion sites. The su(Hw) protein was essential for this enhanced dosage compensation because in a su(Hw) mutant background compensation was incomplete. These experiments provide evidence that the su(Hw)-binding region facilitates dosage compensation of the mini-white gene on the autosomes. This may result from protection of the mini-white gene from a negative autosomal chromatin environment.


PLoS ONE ◽  
2018 ◽  
Vol 13 (10) ◽  
pp. e0205538 ◽  
Author(s):  
Mukesh Maharjan ◽  
Robert K. Maeda ◽  
François Karch ◽  
Craig M. Hart

GeroPsych ◽  
2014 ◽  
Vol 27 (4) ◽  
pp. 161-169 ◽  
Author(s):  
Nienke A. Hofrichter ◽  
Sandra Dick ◽  
Thomas G. Riemer ◽  
Carsten Schleussner ◽  
Monique Goerke ◽  
...  

Hippocampal dysfunction and deficits in episodic memory have been reported for both Alzheimer’s disease (AD) and major depressive disorder (MDD). Primacy performance has been associated with hippocampus-dependent episodic memory, while recency may reflect working memory performance. In this study, serial position profiles were examined in a total of 73 patients with MDD, AD, both AD and MDD, and healthy controls (HC) by means of CERAD-NP word list memory. Primacy performance was most impaired in AD with comorbid MDD, followed by AD, MDD, and HC. Recency performance, on the other hand, was comparable across groups. These findings indicate that primacy in AD is impaired in the presence of comorbid MDD, suggesting additive performance decrements in this specific episodic memory function.


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