Molecular physiology of osmoregulation in eels and other teleosts: the role of transporter isoforms and gene duplication

To gain insight into the mechanism(s) by which cells sense volume changes, specific predictions of the macromolecular crowding theory (A. P. Minton. In: Cellular and Molecular Physiology of Cell Volume Regulation, edited by K. Strange. Boca Raton, FL: CRC, 1994, p. 181-190. A. P. Minton, C. C. Colclasure, and J. C. Parker. Proc. Natl. Acad. Sci. USA 89: 10504-10506, 1992) were tested on the volume of internally perfused barnacle muscle cells. This preparation was chosen because it allows assessment of the effect on cell volume of changes in the intracellular macromolecular concentration and size while maintaining constant the ionic strength, membrane stretch, and osmolality. The predictions tested were that isotonic replacement of large macromolecules by smaller ones should induce volume decreases proportional to the initial macromolecular concentration and size as well as to the magnitude of the concentration reduction. The experimental results were consistent with these predictions: isotonic replacement of proteins or polymers with sucrose induced volume reductions, but this effect was only observed when the replacement was > or = 25% and the particular macromolecule had an average molecular mass of < or = 20 kDa and a concentration of at least 18 mg/ml. Volume reduction was effected by a mechanism identical with that of hypotonicity-induced regulatory volume decrease, namely, activation of verapamil-sensitive Ca2+ channels.

Download Full-text

Gene duplication and rate variation in the evolution of non-photosynthetic pathways in plastids

10.1101/2021.09.13.460099 ◽

2021 ◽

Author(s):

Alissa M Williams ◽

Olivia G Carter ◽

Evan S Forsythe ◽

Hannah K Mendoza ◽

Daniel B Sloan

Keyword(s):

Gene Duplication ◽

Fatty Acid Biosynthesis ◽

Single Copy ◽

Rate Variation ◽

Sequence Evolution ◽

Catalytic Core ◽

Multiple Species ◽

Insight Into ◽

Paralogous Proteins

While the chloroplast (plastid) is known for its role in photosynthesis, it is also involved in many other biosynthetic pathways essential for plant survival. As such, plastids contain an extensive suite of enzymes required for non-photosynthetic processes. The evolution of the associated genes has been especially dynamic in flowering plants (angiosperms), including examples of gene duplication and extensive rate variation. We examined the role of ongoing gene duplication in two key plastid enzymes, the acetyl-CoA carboxylase (ACCase) and the caseinolytic protease (Clp), responsible for fatty acid biosynthesis and protein turnover, respectively. In plants, there are two ACCase complexes: a homomeric version present in the cytosol and a heteromeric version present in the plastid. Duplications of the nuclear-encoded homomeric ACCase gene and retargeting to the plastid have been previously reported in multiple species. We find that these retargeted copies of the homomeric ACCase gene exhibit elevated rates of sequence evolution, consistent with neofunctionalization and/or relaxation of selection. The plastid Clp complex catalytic core is composed of nine paralogous proteins that arose via ancient gene duplication in the cyanobacterial/plastid lineage. We show that further gene duplication occurred more recently in the nuclear-encoded core subunits of this complex, yielding additional paralogs in many species of angiosperms. Moreover, in six of eight cases, subunits that have undergone recent duplication display increased rates of sequence evolution relative to those that have remained single copy. We also compared rate patterns between pairs of Clp core paralogs to gain insight into post-duplication evolutionary routes. These results show that gene duplication and rate variation continue to shape the plastid proteome.

Download Full-text

Horizontal gene transfer as an indispensable driver for Neocallimastigomycota evolution into a distinct gut-dwelling fungal lineage

10.1101/487215 ◽

2018 ◽

Cited By ~ 2

Author(s):

Chelsea L. Murphy ◽

Noha H. Youssef ◽

Radwa A. Hanafy ◽

MB Couger ◽

Jason E. Stajich ◽

...

Keyword(s):

Gene Transfer ◽

Horizontal Gene Transfer ◽

Gene Duplication ◽

Substrate Utilization ◽

High Rank ◽

Eukaryotic Lineage ◽

Fungal Lineage ◽

Fermentative Bacteria ◽

Survival And Growth

AbstractSurvival and growth of the anaerobic gut fungi (AGF, Neocallimastigomycota) in the herbivorous gut necessitate the possession of multiple abilities absent in other fungal lineages. We hypothesized that horizontal gene transfer (HGT) was instrumental in forging the evolution of AGF into a phylogenetically distinct gut-dwelling fungal lineage. Patterns of HGT were evaluated in the transcriptomes of 27 AGF strains, 22 of which were isolated and sequenced in this study, and 4 AGF genomes broadly covering the breadth of AGF diversity. We identified 283 distinct incidents of HGT in AGF transcriptomes, with subsequent gene duplication resulting in an HGT frequency of 2.1-3.6% in AGF genomes. The majority of HGT events were AGF specific (91.5%) and wide (70.7%), indicating their occurrence at early stages of AGF evolution. The acquired genes allowed AGF to expand their substrate utilization range, provided new venues for electron disposal, augmented their biosynthetic capabilities, and facilitated their adaptation to anaerobiosis. The majority of donors were anaerobic fermentative bacteria prevalent in the herbivorous gut. This work strongly indicates that HGT indispensably forged the evolution of AGF as a distinct fungal phylum and provides a unique example of the role of HGT in shaping the evolution of a high rank taxonomic eukaryotic lineage.ImportanceThe anaerobic gut fungi (AGF) represent a distinct basal phylum lineage (Neocallimastigomycota) commonly encountered in the rumen and alimentary tracts of herbivores. Survival and growth of anaerobic gut fungi in these anaerobic, eutrophic, and prokaryotes dominated habitats necessitates the acquisition of several traits absent in other fungal lineages. This manuscript assesses the role of horizontal gene transfer as a relatively fast mechanism for trait acquisition by the Neocallimastigomycota post sequestration in the herbivorous gut. Analysis of twenty-seven transcriptomes that represent the broad Neocallimastigomycota diversity identified 283 distinct HGT events, with subsequent gene duplication resulting in an HGT frequency of 2.1-3.6% in AGF genomes. These HGT events have allowed AGF to survive in the herbivorous gut by expanding their substrate utilization range, augmenting their biosynthetic pathway, providing new routes for electron disposal by expanding fermentative capacities, and facilitating their adaptation to anaerobiosis. HGT in the AGF is also shown to be mainly a cross-kingdom affair, with the majority of donors belonging to the bacteria. This work represents a unique example of the role of HGT in shaping the evolution of a high rank taxonomic eukaryotic lineage.

Download Full-text

Genome-wide characterization of the rose (Rosa chinensis) WRKY family and role of RcWRKY41 in gray mold resistance

10.21203/rs.2.14147/v3 ◽

2019 ◽

Author(s):

Xintong Liu ◽

Dandan Li ◽

Shiya Zhang ◽

Yaling Xu ◽

Zhao Zhang

Keyword(s):

Gene Duplication ◽

Regulatory Gene ◽

Purifying Selection ◽

Gray Mold ◽

Rosa Chinensis ◽

Genome Wide ◽

A Genome ◽

Mold Resistance ◽

The Rose

Abstract Background The WRKYs are a major family of plant transcription factors that play roles in the responses to biotic and abiotic stresses; however, a comprehensive study of the WRKY family in roses ( Rosa sp.) has not previously been performed.Results In the present study, we performed a genome-wide analysis of the WRKY genes in the rose ( Rosa chinensis ), including their phylogenetic relationships, gene structure, chromosomal locations, and collinearity. Using a phylogenetic analysis, we divided the 56 RcWRKY genes into three subgroups. The RcWRKY s were unevenly distributed across all seven rose chromosomes, and a study of their collinearity suggested that genome duplication may have played a major role in RcWRKY gene duplication. A Ka/Ks analysis indicated that they mainly underwent purifying selection. Botrytis cinerea infection induced the expression of 19 RcWRKY s, most of which had undergone gene duplication during evolution. These RcWRKY s may regulate rose resistance against B. cinerea . Based on our phylogenetic and expression analyses, RcWRKY41 was identified as a candidate regulatory gene in the response to B. cinerea infection, which was confirmed using virus-induced gene silencing.Conclusions This study provides useful information to facilitate the further study of the function of the rose WRKY gene family.

Download Full-text

Genome-wide characterization of the rose (Rosa chinensis) WRKY family and role of RcWRKY41 in gray mold resistance

10.21203/rs.2.14147/v1 ◽

2019 ◽

Author(s):

Xintong Liu ◽

Dandan Li ◽

Shiya Zhang ◽

Yaling Xu ◽

Zhao Zhang

Keyword(s):

Gene Duplication ◽

Regulatory Gene ◽

Purifying Selection ◽

Gray Mold ◽

Rosa Chinensis ◽

Genome Wide ◽

A Genome ◽

Mold Resistance ◽

The Rose

Abstract Background The WRKYs are a major family of plant transcription factors that play roles in the responses to biotic and abiotic stresses; however, a comprehensive study of the WRKY family in roses (Rosa sp.) has not previously been performed.Results In the present study, we performed a genome-wide analysis of the WRKY genes in the rose (Rosa chinensis), including their phylogenetic relationships, gene structure, chromosomal locations, and collinearity. Using a phylogenetic analysis, we divided the 56 RcWRKY genes into three subgroups. The RcWRKYs were unevenly distributed across all seven rose chromosomes, and a study of their collinearity suggested that genome duplication may have played a major role in RcWRKY gene duplication. A Ka/Ks analysis indicated that they mainly underwent purifying selection. Botrytis cinerea infection induced the expression of 19 RcWRKYs, most of which had undergone gene duplication during evolution. These RcWRKYs may regulate rose resistance against B. cinerea. Based on our phylogenetic and expression analyses, RcWRKY41 was identified as a candidate regulatory gene in the response to B. cinerea infection, which was confirmed using virus-induced gene silencing.Conclusions This study provides useful information to facilitate the further study of the function of the rose WRKY gene family.

Download Full-text

Why the mechanisms of biological evolution are still not revealed?

Current Research in Biochemistry and Molecular Biology ◽

10.33702/crbmb.2020.1.1.1 ◽

2020 ◽

Vol 2 (1) ◽

pp. 1-8

Author(s):

Abyt Ibraimov

Keyword(s):

Natural Selection ◽

Gene Duplication ◽

Biological Evolution ◽

Gene Mutations ◽

Eukaryotic Genome ◽

Biological Variability ◽

Gene Recombination ◽

Human Chromosomes ◽

Main Obstacle

Since the days of Darwin, it is generally accepted that biological evolution rests on three pillars: variability, inheritance and selection. It is believed that main sources of variability, mechanisms of inheritance and forms of natural selection have been clarified. Nevertheless, for more than 150 years since the publication of “Origin of Species” no consensus as to the mechanisms of evolution emerged. It is highly likely that the main obstacle in elucidating the mechanisms of evolution is the incompleteness of our knowledge regarding the sources of biological variability. The following sources of variability are universally recognized: gene mutations, gene recombination during meiosis and gene duplication. However, the role of the non-genic part of the genome, which makes up the vast majority of DNA in eukaryotes, remains unclear. For example, in human chromosomes, about 98% of DNA is represented by non-coding nucleotide sequences (ncDNAs). Although no one excludes their possible role in evolution, nevertheless, studies aimed at elucidating the participation of the non-genic part of the genome in variability, inheritance and selection are extremely small. The possible role of ncDNAs in the origin of biological variability in the eukaryotic genome and their evolution is discussed.

Download Full-text

Lithium: a versatile tool for understanding renal physiology

AJP Renal Physiology ◽

10.1152/ajprenal.00718.2012 ◽

2013 ◽

Vol 304 (9) ◽

pp. F1139-F1149 ◽

Cited By ~ 48

Author(s):

Bellamkonda K. Kishore ◽

Carolyn M. Ecelbarger

Keyword(s):

Diabetes Insipidus ◽

Glycogen Synthase ◽

Purinergic Signaling ◽

Collecting Duct ◽

Renal Physiology ◽

Urinary Concentration ◽

Paradigm Shifts ◽

Molecular Physiology ◽

Versatile Tool

By virtue of its unique interactions with kidney cells, lithium became an important research tool in renal physiology and pathophysiology. Investigators have uncovered the intricate relationships of lithium with the vasopressin and aldosterone systems, and the membrane channels or transporters regulated by them. While doing so, their work has also led to 1) questioning the role of adenylyl cyclase activity and prostaglandins in lithium-induced suppression of aquaporin-2 gene transcription; 2) unraveling the role of purinergic signaling in lithium-induced polyuria; and 3) highlighting the importance of the epithelial sodium channel (ENaC) in lithium-induced nephrogenic diabetes insipidus (NDI). Lithium-induced remodeling of the collecting duct has the potential to shed new light on collecting duct remodeling in disease conditions, such as diabetes insipidus. The finding that lithium inhibits glycogen synthase kinase-3β (GSK3β) has opened an avenue for studies on the role of GSK3β in urinary concentration, and GSK isoforms in renal development. Finally, proteomic and metabolomic profiling of the kidney and urine in rats treated with lithium is providing insights into how the kidney adapts its metabolism in conditions such as acquired NDI and the multifactorial nature of lithium-induced NDI. This review provides state-of-the-art knowledge of lithium as a versatile tool for understanding the molecular physiology of the kidney, and a comprehensive view of how this tool is challenging some of our long-standing concepts in renal physiology, often with paradigm shifts, and presenting paradoxical situations in renal pathophysiology. In addition, this review points to future directions in research where lithium can lead the renal community.

Download Full-text

Proceedings of the Symposium ‘Angiotensin AT1 Receptors: From Molecular Physiology to Therapeutics’: ROLE OF AT1 RECEPTORS IN THE CENTRAL CONTROL OF SYMPATHETIC VASOMOTOR FUNCTION

Clinical and Experimental Pharmacology and Physiology ◽

10.1111/j.1440-1681.1996.tb02820.x ◽

1996 ◽

Vol 23 (S3) ◽

pp. 93-98 ◽

Cited By ~ 57

Author(s):

Geoffrey A Head

Keyword(s):

Central Control ◽

Molecular Physiology ◽

At1 Receptors ◽

Vasomotor Function

Download Full-text

Chasing cardiac physiology and pathology down the CaMKII cascade

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.00007.2015 ◽

2015 ◽

Vol 308 (10) ◽

pp. H1177-H1191 ◽

Cited By ~ 46

Author(s):

Alicia Mattiazzi ◽

Rosana A. Bassani ◽

Ariel L. Escobar ◽

Julieta Palomeque ◽

Carlos A. Valverde ◽

...

Keyword(s):

Transcriptional Activation ◽

Ischemia Reperfusion Injury ◽

Ischemia Reperfusion ◽

Mechanical Activity ◽

Relaxation Processes ◽

Cardiac Physiology ◽

Molecular Physiology ◽

Intracellular Ca ◽

Dependent Protein

Calcium dynamics is central in cardiac physiology, as the key event leading to the excitation-contraction coupling (ECC) and relaxation processes. The primary function of Ca2+ in the heart is the control of mechanical activity developed by the myofibril contractile apparatus. This key role of Ca2+ signaling explains the subtle and critical control of important events of ECC and relaxation, such as Ca2+ influx and SR Ca2+ release and uptake. The multifunctional Ca2+-calmodulin-dependent protein kinase II (CaMKII) is a signaling molecule that regulates a diverse array of proteins involved not only in ECC and relaxation but also in cell death, transcriptional activation of hypertrophy, inflammation, and arrhythmias. CaMKII activity is triggered by an increase in intracellular Ca2+ levels. This activity can be sustained, creating molecular memory after the decline in Ca2+ concentration, by autophosphorylation of the enzyme, as well as by oxidation, glycosylation, and nitrosylation at different sites of the regulatory domain of the kinase. CaMKII activity is enhanced in several cardiac diseases, altering the signaling pathways by which CaMKII regulates the different fundamental proteins involved in functional and transcriptional cardiac processes. Dysregulation of these pathways constitutes a central mechanism of various cardiac disease phenomena, like apoptosis and necrosis during ischemia/reperfusion injury, digitalis exposure, post-acidosis and heart failure arrhythmias, or cardiac hypertrophy. Here we summarize significant aspects of the molecular physiology of CaMKII and provide a conceptual framework for understanding the role of the CaMKII cascade on Ca2+ regulation and dysregulation in cardiac health and disease.

Download Full-text