Evolutionary shifts in gene expression decoupled from gene duplication across functionally distinct spider silk glands

ABSTRACT Gene duplication is considered an important evolutionary mechanism. Unlike many characterized species, the fission yeast Schizosaccharomyces pombe contains two paralogous genes, tup11 + and tup12 + , that encode transcriptional corepressors similar to the well-characterized budding yeast Tup1 protein. Previous reports have suggested that Tup11 and Tup12 proteins play redundant roles. Consistently, we show that the two Tup proteins can interact together when expressed at normal levels and that each can independently interact with the Ssn6 protein, as seen for Tup1 in budding yeast. However, tup11 − and tup12 − mutants have different phenotypes on media containing KCl and CaCl2. Consistent with the functional difference between tup11 − and tup12 − mutants, we identified a number of genes in genome-wide gene expression experiments that are differentially affected by mutations in the tup11 + and tup12 + genes. Many of these genes are differentially derepressed in tup11 − mutants and are over-represented in genes that have previously been shown to respond to a range of different stress conditions. Genes specifically derepressed in tup12 − mutants require the Ssn6 protein for their repression. As for Tup12, Ssn6 is also required for efficient adaptation to KCl- and CaCl2-mediated stress. We conclude that Tup11 and Tup12 are at least partly functionally diverged and suggest that the Tup12 and Ssn6 proteins have adopted a specific role in regulation of the stress response.

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Mesotocin Gene Expression and Evidence of Gene Duplication in the Tammar Wallaby

Annals of the New York Academy of Sciences ◽

10.1111/j.1749-6632.1998.tb10829.x ◽

1998 ◽

Vol 839 (1 TRENDS IN COM) ◽

pp. 447-449 ◽

Cited By ~ 4

Author(s):

LAURA J. PARRY ◽

ROSS A.D. BATHGATE ◽

RICHARD IVELL

Keyword(s):

Gene Expression ◽

Gene Duplication ◽

Tammar Wallaby

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Evolution of H3K27me3-marked chromatin is linked to gene expression evolution and to patterns of gene duplication and diversification

Genome Research ◽

10.1101/gr.162008.113 ◽

2014 ◽

Vol 24 (7) ◽

pp. 1115-1124 ◽

Cited By ~ 16

Author(s):

R. K. Arthur ◽

L. Ma ◽

M. Slattery ◽

R. F. Spokony ◽

A. Ostapenko ◽

...

Keyword(s):

Gene Expression ◽

Gene Duplication ◽

Expression Evolution ◽

Gene Expression Evolution

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Genes relocated between Drosophila chromosome arms evolve under relaxed selective constraints relative to non-relocated genes

10.1101/178582 ◽

2017 ◽

Author(s):

Margaret L. I. Hart ◽

Ban L. Vu ◽

Quinten Bolden ◽

Keith T. Chen ◽

Casey L. Oakes ◽

...

Keyword(s):

Gene Expression ◽

Population Genetics ◽

Comparative Genomics ◽

Gene Duplication ◽

Male Fertility ◽

Chromosomal Location ◽

Single Copy ◽

Duplicated Genes ◽

Selective Constraints ◽

Functional Analyses

AbstractGene duplication creates a second copy of a gene either in tandem to the ancestral locus or dispersed to another chromosomal location. When the ancestral copy of a dispersed duplicate is lost from the genome, it creates the appearance that the gene was “relocated” from the ancestral locus to the derived location. Gene relocations may be as common as canonical dispersed duplications in which both the ancestral and derived copies are retained. Relocated genes appear to be under more selective constraints than the derived copies of canonical duplications, and they are possibly as conserved as single-copy non-relocated genes. To test this hypothesis, we combined comparative genomics, population genetics, gene expression, and functional analyses to assess the selection pressures acting on relocated, duplicated, and non-relocated single-copy genes in Drosophila genomes. We find that relocated genes evolve faster than single-copy non-relocated genes, and there is no evidence that this faster evolution is driven by positive selection. In addition, relocated genes are less essential for viability and male fertility than single-copy non-relocated genes, suggesting that relocated genes evolve fast because of relaxed selective constraints. However, relocated genes evolve slower than the derived copies of canonical dispersed duplicated genes. We therefore conclude that relocated genes are under more selective constraints than canonical duplicates, but are not as conserved as single-copy non-relocated genes.

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GENETIC AND DEVELOPMENTAL ANALYSIS OF SOME NEW COLOR MUTANTS IN THE GOLDFISH, CARASSIUS AURATUS

Genetics ◽

10.1093/genetics/86.1.161 ◽

1977 ◽

Vol 86 (1) ◽

pp. 161-174

Author(s):

Takao Kajishima

Keyword(s):

Gene Expression ◽

Experimental Data ◽

Gene Duplication ◽

Carassius Auratus ◽

Autosomal Gene ◽

Crossing Experiments ◽

Goldfish Carassius Auratus ◽

Color Mutant ◽

The Common ◽

Developmental Analysis

ABSTRACT The genotypes of three color mutants in goldfish: a depigmentation character of larval melanophores, albinism and a recessive-transparent character, were analyzed by crossing experiments. The depigmentation character in the common goldfish is controlled by two dominant multiple genes, Dp 1 and Dp2, and only fish with double recessive alleles dp1dp1 dp2dp2 can retain larval melanophores throughout life. Albinism is also controlled by double autosomal genes, p and c. The genotype of an albino fish is represented by pp cc; the non-albino fish is PP CC. Fish with either a pp CC or pp Cc genotype are albino when scored at the time of melanosome differentiation in the pigment retina, but after the time of skin melanophore differentiation, they change to the nonalbino type under the control of the C gene. The recessive-transparent character is controlled by a single autosomal gene, g. The mechanisms of gene expression of these characters were proposed as a result of observation and/or experimental data on the differentiation processes of their phenotypes, and the genotypes of these color mutant goldfish were considered in relation to the "gene duplication hypothesis in the Cyprinidae."

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Learning retention mechanisms and evolutionary parameters of duplicate genes from their expression data

10.1101/2020.06.19.162107 ◽

2020 ◽

Author(s):

Michael DeGiorgio ◽

Raquel Assis

Keyword(s):

Gene Expression ◽

Gene Duplication ◽

Statistical Learning ◽

Gene Evolution ◽

Functional Divergence ◽

Duplicate Gene ◽

Duplicate Genes ◽

Evolutionary Mechanisms ◽

Retention Mechanisms ◽

Gene Copies

AbstractLearning about the roles that duplicate genes play in the origins of novel phenotypes requires an understanding of how their functions evolve. To date, only one method—CDROM—has been developed with this goal in mind. In particular, CDROM employs gene expression distances as proxies for functional divergence, and then classifies the evolutionary mechanisms retaining duplicate genes from comparisons of these distances in a decision tree framework. However, CDROM does not account for stochastic shifts in gene expression or leverage advances in contemporary statistical learning for performing classification, nor is it capable of predicting the underlying parameters of duplicate gene evolution. Thus, here we develop CLOUD, a multi-layer neural network built upon a model of gene expression evolution that can both classify duplicate gene retention mechanisms and predict their underlying evolutionary parameters. We show that not only is the CLOUD classifier substantially more powerful and accurate than CDROM, but that it also yields accurate parameter predictions, enabling a better understanding of the specific forces driving the evolution and long-term retention of duplicate genes. Further, application of the CLOUD classifier and predictor to empirical data from Drosophila recapitulates many previous findings about gene duplication in this lineage, showing that new functions often emerge rapidly and asymmetrically in younger duplicate gene copies, and that functional divergence is driven by strong natural selection. Hence, CLOUD represents the best available method for classifying retention mechanisms and predicting evolutionary parameters of duplicate genes, thereby also highlighting the utility of incorporating sophisticated statistical learning techniques to address long-standing questions about evolution after gene duplication.

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Optimization of Spider Silk Glands for the Elicited Production of a Tissue‐Specific Fibroin Product

The FASEB Journal ◽

10.1096/fasebj.20.4.a105-c ◽

2006 ◽

Vol 20 (4) ◽

Author(s):

Brenda Marie Marrero ◽

Ivelisse Cajigas ◽

Xiomara Cajigas ◽

Shadia Medina ◽

Marcos Llavona ◽

...

Keyword(s):

Spider Silk ◽

Tissue Specific ◽

Silk Glands

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Mouse homeo-genes within a subfamily, Hox-1.4, -2.6 and -5.1, display similar anteroposterior domains of expression in the embryo, but show stage- and tissue-dependent differences in their regulation

Development ◽

10.1242/dev.107.1.131 ◽

1989 ◽

Vol 107 (1) ◽

pp. 131-141 ◽

Cited By ~ 13

Author(s):

S.J. Gaunt ◽

R. Krumlauf ◽

D. Duboule

Keyword(s):

Gene Expression ◽

Central Nervous System ◽

Nervous System ◽

In Situ Hybridization ◽

Gene Duplication ◽

Selective Advantage ◽

New Findings ◽

The Central Nervous System ◽

Embryo Sections

By use of in situ hybridization experiments on mouse embryo sections, we compare the transcript patterns of three homeo-genes from the Hox-1.4 subfamily (Hox-1.4, -2.6 and -5.1). Genes within a subfamily are true homologues, present in the genome as a result of duplication of an ancestral homeo-gene cluster. We show that Hox-1.4, -2.6 and -5.1 are similar, although apparently not identical, in the limits of their transcript domains along the anteroposterior axis. Within the prevertebral column of the 12 1/2 day embryo, for example, the anterior boundary of transcripts for each of the three genes was most obvious at the junction of the first and second prevertebrae. Similarly, all three genes showed an anterior boundary of transcripts within the central nervous system that was located in the mid-myelencephalon of the hindbrain. Both in the prevertebral column and hindbrain, however, Hox-2.6 and Hox-5.1 transcripts extended slightly anterior to the anteriormost limits detected for Hox-1.4. In spite of close similarities in the positions of their transcript domains, Hox-1.4, -2.6 and -5.1 displayed striking stage- and tissue-dependent differences in the relative abundance of their transcripts. For example, Hox-5.1 transcripts were abundant within mesoderm and ectoderm of early stages (8 1/2 and 9 1/2 days), yet were detected only weakly in mesodermal components of the lung and stomach at 10 1/2 days, and were apparently absent from these tissues at 12 1/2 days. In contrast, Hox-1.4 and Hox-2.6 transcripts were relatively weakly detected at 8 1/2 and 9 1/2 days, but were abundant within the lung and stomach at 12 1/2 days. Our findings suggest, but do not prove, that genes within the Hox-1.4 subfamily might be coordinately regulated in their expression. We discuss the patterns of mouse homeo-gene expression now observed in terms of models originally devised for Drosophila. We also propose how our new findings may help to explain any selective advantage to the vertebrates of homeo-gene duplication to form subfamilies.

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Low Level Amplification (Duplication) of 1q21 in Myeloma and Prognosis; the Role of CKS1B.

Blood ◽

10.1182/blood.v106.11.624.624 ◽

2005 ◽

Vol 106 (11) ◽

pp. 624-624

Author(s):

Rafael Fonseca ◽

Scott Van Wier ◽

Wee-Joo Chng ◽

Rhett Ketterling ◽

Martha Lacy ◽

...

Keyword(s):

Gene Expression ◽

Cell Cycle ◽

Gene Duplication ◽

Plasma Cell ◽

Plasma Cells ◽

Prognostic Significance ◽

Positive Association ◽

Gene Copy ◽

High Dose ◽

Control Probe

Abstract Introduction: Molecular cytogenetic studies have revealed that, to a great extent, the heterogeneity of myeloma is largely dictated by the underlying genetic and cytogenetic aberrations present in the clonal plasma cells. Most recently the group from the University of Arkansas identified strong prognostic associations with an increased level of gene expression of a cell cycle associated gene, CKS1B. CKS1B favors cell cycle progression by promoting degradation of p27 with release of the cyclin dependent kinases and entry into mitosis. Patients and methods: To further test this hypothesis we studied: a) via FISH for CKS1B amplification in a cohort of patients treated at the Mayo Clinic with high dose chemotherapy and stem cell support, as well as a group of patients with cytogenetically defined hypodiploidy, and b) a cohort of myeloma patients that were studied by gene expression profiling. Gene expression analysis was performed on CD138-enriched plasma-cell RNA using Affymetrix U133A chips (Affymetrix, Santa Clara, CA). Results: Of 159 patients studied 46 exhibited FISH abnormalities consistent with increase number of signals for CKS1B (30%): amplification was marginal or low in 44 cases, and in only two cases the ratio between CKS1B and control probe was greater than 2.0. Therefore, the predominant pattern is one of gene duplication rather than amplification where gene copy usually exceeds 10 and ratio with control probe exceeds 5 (e.g. HER-2/neu amplification). Patients with CKS1B duplication had a higher prevalence of chromosome 13 deletion (72%), and t(4;14) (29%). The presence of CKS1B duplication was more frequent (53%) among 19 patients with hypodiploidy. Using gene expression data for CKS1B, we found a positive association with t(14;16)(q32;q23). The level of CKS1B gene expression positively correlated with the PCLI (p<0.0001) but there was heterogeneity in this relationship (r2 = 0.34). We found no correlation between the expression level of CKS1B and p27 (r2 = 0.008, p = 0.37). While CKS1B gene duplication had a negative effect on survival this effect was weak (29.9 versus 38 months, p = 0.124. Median follow-up is 55 months) and disappeared when the variable was entered into the multivariate model including PCLI, B2-microglobulin and all the major genetic abnormalities by FISH. Likewise the level of expression of CKS1B determined by gene expression only carried prognostic significance when extreme levels of expression were utilized as a prognostic variable. Discussion: In this study we show that increase copy number of CKS1B is present in one third of patients with MM (majority of these being gene duplication) and seem to be associated with a shorter overall survival, but the net effect of this is rather weak in our series. Further study is needed to understand its potential role as a progression factor in the plasma cell neoplasms.

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