Gene dosage affects the expression of the duplicated NHP6 genes of Saccharomyces cerevisiae

Kolodrubetz, David J; Kruppa, Michael; Burgum, Alex

doi:10.1016/s0378-1119(01)00568-6

Cited by 19 publications

(19 citation statements)

References 28 publications

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“…The WGD paralogs NHP6A and NHP6B, which share 89% sequence identity, are an example of this phenomenon. Deletion of NHP6A leads to a threefold increase in NHP6B synthesis while an extra copy of NHP6A reduces NHP6B expression twofold (Kolodrubetz et al 2001). Changes in the NHP6B gene copy number cause similar but more moderate changes in NHP6A expression (Kolodrubetz et al 2001).…”

Section: Discussionmentioning

confidence: 99%

“…Deletion of NHP6A leads to a threefold increase in NHP6B synthesis while an extra copy of NHP6A reduces NHP6B expression twofold (Kolodrubetz et al 2001). Changes in the NHP6B gene copy number cause similar but more moderate changes in NHP6A expression (Kolodrubetz et al 2001). However, such enhanced expression of one gene in response to deletion of its paralog may not be a general pattern in either the WGD or the SSD sets on the basis of our analysis of genomewide expression data in deletion strains (Hughes et al 2000) (supplemental Figure S8 at http://www.genetics.org/ supplemental/).…”

Section: Discussionmentioning

confidence: 99%

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Functional Analysis of Gene Duplications in Saccharomyces cerevisiae

Guan¹,

Dunham²,

2007

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Gene duplication can occur on two scales: whole-genome duplications (WGD) and smaller-scale duplications (SSD) involving individual genes or genomic segments. Duplication may result in functionally redundant genes or diverge in function through neofunctionalization or subfunctionalization. The effect of duplication scale on functional evolution has not yet been explored, probably due to the lack of global knowledge of protein function and different times of duplication events. To address this question, we used integrated Bayesian analysis of diverse functional genomic data to accurately evaluate the extent of functional similarity and divergence between paralogs on a global scale. We found that paralogs resulting from the whole-genome duplication are more likely to share interaction partners and biological functions than smaller-scale duplicates, independent of sequence similarity. In addition, WGD paralogs show lower frequency of essential genes and higher synthetic lethality rate, but instead diverge more in expression pattern and upstream regulatory region. Thus, our analysis demonstrates that WGD paralogs generally have similar compensatory functions but diverging expression patterns, suggesting a potential of distinct evolutionary scenarios for paralogs that arose through different duplication mechanisms. Furthermore, by identifying these functional disparities between the two types of duplicates, we reconcile previous disputes on the relationship between sequence divergence and expression divergence or essentiality.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Functional Analysis of Gene Duplications in Saccharomyces cerevisiae

Guan¹,

Dunham²,

2007

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“…Nhp6 has a single HMG box motif related to the HMGB family of abundant, conserved chromatin factors (1,4). Nhp6 binds to DNA and to nucleosomes (11,25), and both enhance sensitivity to DNase I at specific sites in nucleosomes and also allow formation of yFACT⅐nucleosome complexes (11).…”

Section: Discussionmentioning

confidence: 99%

“…Nhp6 is a DNA-binding protein that is encoded by two similar genes in Saccharomyces cerevisiae, NHP6A and NHP6B (1). Nhp6A and Nhp6B proteins (93 and 99 total residues, respectively) are 88% identical and functionally redundant (2,3), so we refer here to both as Nhp6 protein.…”

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confidence: 99%

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Multiple Nhp6 Molecules Are Required to Recruit Spt16-Pob3 to Form yFACT Complexes and to Reorganize Nucleosomes

Ruone

Rhoades

Formosa

2003

Journal of Biological Chemistry

108

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The Saccharomyces cerevisiae Nhp6 protein contains a DNA-binding motif that is similar to those found in the high mobility group B family of chromatin proteins. Nhp6 bound to nucleosomes and made at least two changes in them: the nucleosomal DNA became more sensitive to DNase I at specific sites, and the nucleosomes became competent to bind Spt16-Pob3 to form yFACT⅐nucleosome complexes. Both changes occurred at similar concentrations of Nhp6, suggesting that they reflect the same structural reorganization of the nucleosome. Nucleosomes have multiple binding sites for Nhp6, and structural reorganization was associated with a concentration of Nhp6 about 10-fold higher than that needed for simple binding. We propose that the coordinated action of multiple Nhp6 molecules is required to convert nucleosomes to an alternative form as the first step in a two-step reorganization of nucleosomes with the second step being dependent on Spt16-Pob3. The presence of linker DNA had only subtle effects on these processes, indicating that both Nhp6 and yFACT act on core nucleosome structure rather than on the interaction between nucleosomes and adjacent DNA. These results suggest that Nhp6 and the related high mobility group B proteins may have a general role in promoting rearrangements of chromatin by initiating the destabilization of core nucleosomal structure.

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Molecular mechanisms of paralogous compensation and the robustness of cellular networks

Diss¹,

et al. 2013

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Robustness is the ability of a system to maintain its function despite environmental or genetic perturbation. Genetic robustness is a key emerging property of living systems and is achieved notably by the presence of partially redundant parts that result from gene duplication. Functional overlap between paralogs allows them to compensate for each other's loss, as commonly revealed by aggravating genetic interactions. However, the molecular mechanisms linking the genotype (loss of function of a gene) to the phenotype (genetic buffering by a paralog) are still poorly understood and the molecular aspects of this compensation are rarely addressed in studies of gene duplicates. Here, we review molecular mechanisms of functional compensation between paralogous genes, many of which from studies that were not meant to study this phenomenon. We propose a standardized terminology and, depending on whether or not the molecular behavior of the intact gene is modified in response to the deletion of its paralog, we classify mechanisms of compensation into passive and active events. We further describe three non-exclusive mechanisms of active paralogous compensation for which there is evidence in the literature: changes in abundance, in localization, and in protein interactions. This review will serve as a framework for the genetic and molecular analysis of paralogous compensation, one of the universal features of genetic systems.

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Gene dosage affects the expression of the duplicated NHP6 genes of Saccharomyces cerevisiae

Cited by 19 publications

References 28 publications

Functional Analysis of Gene Duplications in Saccharomyces cerevisiae

Functional Analysis of Gene Duplications in Saccharomyces cerevisiae

Multiple Nhp6 Molecules Are Required to Recruit Spt16-Pob3 to Form yFACT Complexes and to Reorganize Nucleosomes

Molecular mechanisms of paralogous compensation and the robustness of cellular networks

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