Preadipocyte conversion to macrophage. Evidence of plasticity

Preadipocytes are present throughout adult life in adipose tissues and can proliferate and differentiate into mature adipocytes according to the energy balance. An increasing number of reports demonstrate that cells from adipose lineages (preadipocytes and adipocytes) and macrophages share numerous functional or antigenic properties. No large scale comparison reflecting the phenotype complexity has been performed between these different cell types until now. We used profiling analysis to define the common features shared by preadipocyte, adipocyte, and macrophage populations. Our analysis showed that the preadipocyte profile is surprisingly closer to the macrophage than to the adipocyte profile. From these data, we hypothesized that in a macrophage environment preadipocytes could effectively be converted into macrophages. We injected labeled stroma-vascular cells isolated from mouse white adipose tissue or 3T3-L1 preadipocyte cell line into the peritoneal cavity of nude mice and investigated changes in their phenotype. Preadipocytes rapidly and massively acquired high phagocytic activity and index. 60-70% of preadipocytes also expressed five macrophage-specific antigens: F4/80, Mac-1, CD80, CD86, and CD45. These values were similar to those observed for peritoneal macrophages. In vitro experiments showed that cell-to-cell contact between preadipocytes and peritoneal macrophages partially induced this preadipocyte phenotype conversion. Overall, these results suggest that preadipocyte and macrophage phenotypes are very similar and that preadipocytes have the potential to be very efficiently and rapidly converted into macrophages. This work emphasizes the great cellular plasticity of adipose precursors and reinforces the link between adipose tissue and innate immunity processes.     

Mitoproteome plasticity of rat brown adipocytes in response to cold acclimation

Cold acclimation induces an adaptative increase in respiration in brown adipose tissue (BAT). A comparative analysis by two-dimensional differential in-gel electrophoresis of mitochondrial protein patterns found in rat control and cold-acclimated BAT was performed. A total of 58 proteins exhibiting significant differences in their abundance was unambiguously identified. Proteins implicated in the major catabolic pathways were up-regulated as were ATP synthase and mitofilin. Moreover, these results support the fact that adipocytes can balance their ATP synthesis and their heat production linked to UCP1-sustained uncoupling.     

Saccharomyces cerevisiae mitoproteome plasticity in response to recombinant alternative ubiquinol oxidase

The energy-dissipating alternative oxidase (AOX) from Hansenula anomala was expressed in Saccharomyces cerevisiae. The recombinant AOX was functional. A comparative analysis by two-dimensional differential in-gel electrophoresis (2D-DIGE) of mitochondrial protein patterns found in wild-type and recombinant AOX strains was performed. 60 proteins exhibiting a significant difference in their abundance were identified. Interestingly, proteins implicated in major metabolic pathways such as Krebs cycle and amino acid biosynthesis were up-regulated. Surprisingly, an up-regulation of the respiratory-chain complex III was associated with a down-regulation of the ATP synthase complex.     

Genome plasticity in Neisseria gonorrhoeae

Abstract The pathogenic Neisseria have exploited the processes of horizontal DNA transfer and genetic recombination as mechanisms for the generation of extensive protein variation and modulation of gene expression. Localized recombinations have been well documented in members of multigene families as have alterations in short repetitive sequences. Here we report an analysis of the chromosomal structure of a defined lineage of Neisseria gonorrhoeae strain MS 11 pilin variants. This study reveals the occurrence of large rearrangements, including the amplification of a 26 kb region and an inversion involving more than a third of the chromosome. Additionally, a restriction site polymorphism that correlates with pilin expression has been observed. These findings highlight the flexibility of the gonococcal genome.     

Synaptic signalling in cerebellar plasticity

A major goal of learning and memory research is to correlate the function of molecules with the behaviour of organisms. The beautiful laminar structure of the cerebellar cortex lends itself to the study of synaptic plasticity, because its clearly defined patterns of neurons and their synapses form circuits that have been implicated in simple motor behaviour paradigms. The best understood in terms of molecular mechanism is the parallel fibre-Purkinje cell synapse, where presynaptic long-term potentiation and postsynaptic long-term depression and potentiation finely tune cerebellar output. Our understanding of these forms of plasticity has mostly come from the electrophysiological and behavioural analysis of knockout mutant mice, but more recently the knock-in of synaptic molecules with mutated phosphorylation sites and binding domains has provided more detailed insights into the signalling events. The present review details the major forms of plasticity in the cerebellar cortex, with particular attention to the membrane trafficking and intracellular signalling responsible. This overview of the current literature suggests it will not be long before the involvement of the cerebellum in certain motor behaviours is fully explained in molecular terms.     

Codon bias and plasticity in immunoglobulins

Immunoglobulin genes experience Darwinian evolution twice. In addition to the germline evolution all genes experience, immunoglobulins are subjected, upon exposure to antigen, to somatic hypermutation. This is accompanied by selection for high affinity to the eliciting antigen and frequently results in a significant increase in the specificity of the responding population. The hypermutation mechanism displays a strong sequence specificity. Thus arises the opportunity to manipulate codon bias in a site-specific manner so as to direct hypermutation to those parts of the gene that encode the antigen-binding portions of the molecule and away from those that encode the structurally conserved regions. This segregation of mutability would clearly be advantageous; it would enhance the generation of potentially useful variants while keeping mutational loss to acceptably low levels. But it is not clear that the advantage gained would be large enough to produce a measurable effect within the background stochasticity of the evolutionary process. I have performed a pair of statistical tests to determine whether site- specific codon bias in human immunoglobulin genes is correlated with the sequence specificity of the somatic mutation mechanism. The sequence specificity of the mutator was determined by analysis of a database of published immunoglobulin intron sequences that had experienced somatic mutation but not selection. The site-specific codon bias was determined by analysis of published sequences of human germline immunoglobulin V genes. Both tests strongly suggest that evolution has acted to enhance the plasticity of immunoglobulin genes under somatic hypermutation.      

Cell plasticity in homeostasis and regeneration

Over the past decades, genetic analyses performed in vertebrate and invertebrate organisms deciphered numerous cellular and molecular mechanisms deployed during sexual development and identified genetic circuitries largely shared among bilaterians. In contrast, the functional analysis of the mechanisms that support regenerative processes in species randomly scattered among the animal kingdom, were limited by the lack of genetic tools. Consequently, unifying principles explaining how stress and injury can lead to the reactivation of a complete developmental program with restoration of original shape and function remained beyond reach of understanding. Recent data on cell plasticity suggest that beside the classical developmental approach, the analysis of homeostasis and asexual reproduction in adult organisms provides novel entry points to dissect the regenerative potential of a given species, a given organ or a given tissue. As a clue, both tissue homeostasis and regeneration dynamics rely on the availability of stem cells and/or on the plasticity of differentiated cells to replenish the missing structure. The freshwater Hydra polyp provides us with a unique model system to study the intricate relationships between the mechanisms that regulate the maintenance of homeostasis, even in extreme conditions (starvation and overfeeding) and the reactivation of developmental programs after bisection or during budding. Interestingly head regeneration in Hydra can follow several routes according to the level of amputation, suggesting that indeed the homeostatic background dramatically influences the route taken to bridge injury and regeneration. Mol. Reprod. Dev. 77:837–855, 2010. © 2010 Wiley‐Liss, Inc.     

Contribution of mobile genetic elements to Desulfovibrio vulgaris genome plasticity

The genome of Desulfovibrio vulgaris strain DePue, a sulfate-reducing Deltaproteobacterium isolated from heavy metal-impacted lake sediment, was completely sequenced and compared with the type strain D. vulgaris Hildenborough. The two genomes share a high degree of relatedness and synteny, but harbour distinct prophage and signatures of past phage encounters. In addition to a highly variable phage contribution, the genome of strain DePue contains a cluster of open-reading frames not found in strain Hildenborough coding for the production and export of a capsule exopolysaccharide, possibly of relevance to heavy metal resistance. Comparative whole-genome microarray analysis on four additional D. vulgaris strains established greater interstrain variation within regions associated with phage insertion and exopolysaccharide biosynthesis.     

Developmental plasticity in metabolic rates reinforces morphological plasticity in response to social cues of sexual selection

Developmental plasticity allows individuals to match their phenotype to the competitive environment they are most likely to encounter. Although there are numerous studies that demonstrate adaptive shifts in life-history and metric traits, we still have a poor understanding of whether internal physiological processes demonstrate plasticity and whether this plasticity supports life-history and metric traits. Here we use the Australian redback spider (Latrodectus hasselti), a species that demonstrates adaptive developmental shifts in response to the availability of females and the density of males, to examine the relationship between the routine metabolic rate (RMR) and the expression of size, body-condition and development rate. We reared immature males in three diet treatments, and in social environments that varied the presence/absence of females and the density of males and measured their RMR, weight, size and developmental rate at maturity. We show that although RMR decreased with decreasing resource abundance, RMR was positively correlated with the density of rivals. Moreover, RMR was not correlated with size or body-condition at maturity. Our results demonstrate that plasticity in the RMR supports plasticity in metric and life-history traits to create an integrated phenotype that matches the competitive environment.     

Functional site plasticity in domain superfamilies

We present, to our knowledge, the first quantitative analysis of functional site diversity in homologous domain superfamilies. Different types of functional sites are considered separately. Our results show that most diverse superfamilies are very plastic in terms of the spatial location of their functional sites. This is especially true for protein–protein interfaces. In contrast, we confirm that catalytic sites typically occupy only a very small number of topological locations. Small-ligand binding sites are more diverse than expected, although in a more limited manner than protein–protein interfaces. In spite of the observed diversity, our results also confirm the previously reported preferential location of functional sites. We identify a subset of homologous domain superfamilies where diversity is particularly extreme, and discuss possible reasons for such plasticity, i.e. structural diversity. Our results do not contradict previous reports of preferential co-location of sites among homologues, but rather point at the importance of not ignoring other sites, especially in large and diverse superfamilies. Data on sites exploited by different relatives, within each well annotated domain superfamily, has been made accessible from the CATH website in order to highlight versatile superfamilies or superfamilies with highly preferential sites. This information is valuable for system biology and knowledge of any constraints on protein interactions could help in understanding the dynamic control of networks in which these proteins participate. The novelty of our work lies in the comprehensive nature of the analysis – we have used a significantly larger dataset than previous studies – and the fact that in many superfamilies we show that different parts of the domain surface are exploited by different relatives for ligand/protein interactions, particularly in superfamilies which are diverse in sequence and structure, an observation not previously reported on such a large scale. This article is part of a Special Issue entitled: The emerging dynamic view of proteins: Protein plasticity in allostery, evolution and self-assembly.     

Proteome plasticity in response to persistent environmental change

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Root architecture governs plasticity in response to drought

Aims

Fine root morphological traits are generally changed under soil nitrogen (N) enrichment, however, the underlying mechanism and functional significance are still not well understood. Our aims were to investigate the linkage of root morphology to anatomy, and its implication for root function at elevated soil N availability.

Methods

Ingrowth cores were used to sample root tips (0–20 cm soil depth) from six temperate tree species growing in monoculture plantations at a common site in northeastern China. Root morphological and anatomical traits were concurrently measured, and their relationships were determined within and among species in both control and N fertilization (10 g N m^?2y^?1) plots.

Results

Root diameter generally increased in all six species (non-significant for Phellodendron amurense) following N fertilization, which was caused by the increased root stele radius rather than cortical thickness. Congruently, N fertilization significantly decreased the ratio of cortical thickness to stele radius, but increased the ratio of total cross-sectional area of conduits to stele area in root tips across all species.

Conclusions

The observed anatomical changes of root tips contributed to the alternations of morphological root traits following N fertilization, with potentially important impacts on root physiological functions, like increased water and nutrient transport.

     

Use of genotype-environment interactions to elucidate the pattern of maize root plasticity to nitrogen deficiency

Maize(Zea mays L.) root morphology exhibits a high degree of phenotypic plasticity to nitrogen(N) de ficiency,but the underlying genetic architecture remains to be investigated Using an advanced BC_4F_3 population,we investigated the root growth plasticity under two contrasted N levels and identi fied the quantitative trait loci(QTLs) with QTL-environment(Q×E)interaction effects. Principal components analysis(PCA) on changes of root traits to N de ficiency(D LN-HN) showed that root length and biomass contributed for 45.8% in the same magnitude and direction on the first PC,while root traits scattered highly on PC_2 and PC_3. Hierarchical cluster analysis on traits for D LN-HN further assigned the BC_4F_3 lines into six groups,in which the special phenotypic responses to N de ficiency was presented These results revealed the complicated root plasticity of maize in response to N de ficiency that can be caused by genotype environment(G×E) interactions. Furthermore,QTL mapping using a multi-environment analysis identi fied 35 QTLs for root traits. Nine of these QTLs exhibited signi ficant Q×E interaction effects. Taken together,our findings contribute to understanding the phenotypic and genotypic pattern of root plasticity to N de ficiency,which will be useful for developing maize tolerance cultivars to N de ficiency.     

Tree shape plasticity in relation to crown exposure

Trees outside closed forest stands differ in the relation between stem diameter, height and crown volume from trees that grew with neighbours close by. Whether this plasticity in tree shape varies between species in relation to their light requirement is unknown. We purposefully sampled 528 trees ranging 5–100?cm diameter at breast height growing in a range of light conditions. Across ten broad-leaved species observed in Sumatra or Kalimantan, a generic relationship was found between light exposure of the crown and a light-dependent a _l parameter that modifies the height–diameter allometric equation (H?=?a _l D ^b ) from those for closed stands. In our results, vertical stretching is well predicted by light availability. In fully open conditions, trees are on average 31% shorter for the same diameter than under (partial) shade. Most of the stretching response occurs in all species as soon as some degree of lateral shading occurs. The response, however, varies by species (8–44% reduction) in a way apparently unrelated to species’ successional status. Crown volume varied less than stem height in its relationship with stem diameter across all light conditions tested. The scaling of crown volume with stem diameter, however, differed markedly between tree species.     

Ecological limits to plant phenotypic plasticity

Phenotypic plasticity is considered the major means by which plants cope with environmental heterogeneity. Although ubiquitous in nature, actual phenotypic plasticity is far from being maximal. This has been explained by the existence of internal limits to its expression. However, phenotypic plasticity takes place within an ecological context and plants are generally exposed to multifactor environments and to simultaneous interactions with many species. These external, ecological factors may limit phenotypic plasticity or curtail its adaptive value, but seldom have they been considered because limits to plasticity have typically addressed factors internal to the plant. We show that plastic responses to abiotic factors are reduced under situations of conservative resource use in stressful and unpredictable habitats, and that extreme levels in a given abiotic factor can negatively influence plastic responses to another factor. We illustrate how herbivory may limit plant phenotypic plasticity because damaged plants can only rarely attain the optimal phenotype in the challenging environment. Finally, it is examined how phenotypic changes involved in trait-mediated interactions can entail costs for the plant in further interactions with other species in the community. Ecological limits to plasticity must be included in any realistic approach to understand the evolution of plasticity in complex environments and to predict plant responses to global change.