Reply to Manger’s Commentary on “A quantitative test of the thermogenesis hypothesis of cetacean brain evolution,using phylogenetic comparative methods”

In his Commentary (Manger PR. 2009. Subglacial cetaceans and other mathematical mysteries: a Commentary on “A quantitative test of the thermogenesis hypothesis of cetacean brain evolution, using phylogenetic comparative methods” by C. Maximino. Mar Fresh Behav Physiol. 42: 359–362) on my paper (Maximino C. 2009. A quantitative test of the thermogenesis hypothesis of cetacean brain evolution, using phylogenetic comparative methods. Mar Freshwater Behav Physiol. 42:1–17), Dr Paul Manger noted four errors in the quantitative analysis of the relationship between cetacean encephalization quotients (EQs) and water temperatures, which I suggested was a test of his thermogenesis hypothesis (Manger PR. 2006 Manger, PR. 2006. An examination of cetacean brain structure with a novel hypothesis correlating thermogenesis to the evolution of a big brain. Biol Rev Camb Philos Soc, 81: 293–338.  [Google Scholar]. An examination of cetacean brain structure with a novel hypothesis correlating thermogenesis to the evolution of a big brain. Biol Rev Camb Philos Soc. 81:293–338). These referred to incorrect raw data on water temperatures for two species, odd use of midpoint temperatures as independent variable, lack of inclusion of data on Mysticeti and the use of a differently derived EQ and midpoints instead of the EQs proposed by Manger and temperature ranges; Dr Manger proposed that these errors invalidate the analysis, with special emphasis in an observation that, since my paper did not address the relationship between EQs and temperature range, it did not actually test the thermogenesis hypothesis. In this Reply, I apologize for the mistakes which were made, and show that re-analysis using all the proposed alterations do not qualitatively or quantitatively alter the final result. I also argue that the relationship between phylogenetically correct EQs and midpoint temperatures is a better test of the thermogenesis hypothesis than the relationship between non-phylogenetic EQs and temperature ranges.     

An exact solution of transient equations describing slow axonal transport

An exact analytical solution of equations describing slow axonal transport of cytoskeletal elements (CEs) injected in an axon is presented. The equations modelling slow axonal transport are based on the stop-and-go hypothesis. The simplest model implementing this hypothesis postulates that CEs switch between pausing and running kinetic states, and that the probabilities of CE transition between these two states are described by first-order rate constants. It is assumed that initially CEs are injected such that they form a uniform pulse of a given width. All injected CEs are initially attributed to the pausing state. It is shown that within 30 s kinetic processes redistribute CEs between pausing and running states; after that the process occurs under quasi-equilibrium conditions. The parameter accessible to experiments is the total concentration of CEs (pausing plus running). As the initial rectangular-shaped pulse moves, it changes its shape to become a bell-shaped wave that spreads out as it propagates. The wave's amplitude is decreasing during the wave's propagation. It is also shown that the system forgets its initial condition, meaning that if one starts with pulses of different widths, after sometime they converge to the same bell-shaped wave.     

How independent are TSE agents from their hosts?

Central to understanding the nature TSE agents (or prions) is how their genetic information is distinguished from the host. Are TSEs truly infectious diseases with host-independent genomes, or are they aberrations of a host component derived from the host genome? Recent experiments tested whether glycosylation of host PrP affects TSE strain characteristics. Wild-type mice were infected with 3 TSE strains passaged through transgenic mice with PrP devoid of glycans at 1 or both N-glycosylation sites. Strain-specific characteristics of 1 TSE strain changed but did not change for 2 others. Changes resulted from the selection of mutant TSE strains in a novel replicative environment. In general the properties of established TSEs support the genetic independence of TSE agents from the host, and specifically the primary structure of PrP does not directly encode TSE agent properties. However sporadic TSEs, challenge this independency. The prion hypothesis explains emerging TSEs relatively successfully but poorly accounts for the diversity and mutability of established TSE strains, or how many different infectious conformations are sustained thermodynamically. Research on early changes in RNA expression and events at the ribosome may inform the debate on TSE agent properties and their interaction with host cell machinery.     

榆耳不同极性提取物的体外抑菌活性

采用圆滤纸片法,以金黄色葡萄球菌O41ermc、S19NMA1、ATCC25923和大肠杆菌ERcat、EΠ￡R、ATCC25923为受试菌种,对榆耳石油醚、氯仿、乙酸乙酯、丙酮、甲醇和水不同极性提取物进行抑菌活性研究。结果表明:榆耳不同极性提取物对不同的菌种均有不同程度的抑制作用。     

Biotic and abiotic factors driving the diversification dynamics of Crocodylia

Species diversity patterns are governed by complex interactions among biotic and abiotic factors over time and space, but are essentially the result of the diversification dynamics (differential speciation and extinction rates) over the long-term evolutionary history of a clade. Previous studies have suggested that temporal variation in global temperature drove long-term diversity changes in Crocodylia, a monophyletic group of large ectothermic organisms. We use a large database of crocodylian fossil occurrences (192 spp.) and body mass estimations, under a taxic approach, to characterize the global diversification dynamics of crocodylians since the Cretaceous, and their correlation with multiple biotic and abiotic factors in a Bayesian framework. The diversification dynamic of crocodylians, which appears to have originated in the Turonian (c. 92.5 Ma), is characterized by several phases with high extinction and speciation rates within a predominantly low long-term mean rate. Our results reveal long-term diversification dynamics of Crocodylia to be a highly complex process driven by a combination of biotic and abiotic factors which influenced the speciation and extinction rates in dissimilar ways. Higher crocodylian extinction rates are related to low body mass disparity, indicating selective extinctions of taxa at both ends of the body mass spectrum. Speciation rate slowdowns are noted when the diversity of the clade is high and the warm temperate climatic belt is reduced. Our finding supports the idea that temporal variations of body mass disparity, self-diversity, and the warm climate belt size provided more direct mechanistic explanations for crocodylian diversification than do proxies of global temperature.     

Differential spreading of HinfI satellite DNA variants during radiation in Centaureinae

Background and Aims

Subtribe Centaureinae appears to be an excellent model group in which to analyse satellite DNA and assess the influence that the biology and/or the evolution of different lineages have had on the evolution of this class of repetitive DNA. Phylogenetic analyses of Centaureinae support two main phases of radiation, leading to two major groups of genera of different ages. Furthermore, different modes of evolution are observed in different lineages, reflected by morphology and DNA sequences.

Methods

The sequences of 502 repeat units of the HinfI satellite DNA family from 38 species belonging to ten genera of Centaureinae were isolated and compared. A phylogenetic reconstruction was carried out by maximum likelihood and Bayesian inference.

Key Results

Up to eight different HinfI subfamilies were found, based on the presence of a set of diagnostic positions given by a specific mutation shared by all the sequences of one group. Subfamilies V–VIII were mostly found in older genera (first phase of radiation in the subtribe, late Oligocene–Miocene), although some copies of these types of repeats were also found in some species of the derived genera. Subfamilies I–IV spread mostly in species of the derived clade (second phase of radiation, Pliocene to Pleistocene), although repeats of these subfamilies exist in older species. Phylogenetic trees did not group the repeats by taxonomic affinity, but sequences were grouped by subfamily provenance. Concerted evolution was observed in HinfI subfamilies spread in older genera, whereas no genetic differentiation was found between species, and several subfamilies even coexist within the same species, in recently radiated groups or in groups with a history of recurrent hybridization of lineages.

Conclusions

The results suggest that the eight HinfI subfamilies were present in the common ancestor of Centaureinae and that each spread differentially in different genera during the two main phases of radiation following the library model of satellite DNA evolution. Additionally, differential speciation pathways gave rise to differential patterns of sequence evolution in different lineages. Thus, the evolutionary history of each group of Centaureinae is reflected in HinfI satellite DNA evolution. The data reinforce the value of satellite DNA sequences as markers of evolutionary processes.     

DNA-damage response in chromatin of ribosomal genes and the surrounding genome

DNA repair events have functional significance especially for genome stability. Although the DNA damage response within the whole genome has been extensively studied, the region-specific characteristics of nuclear sub-compartments such as the nucleolus or fragile sites have not been fully elucidated. Here, we show that the heterochromatin protein HP1 and PML protein recognize spontaneously occurring 53BP1- or γ-H2AX-positive DNA lesions throughout the genome. Moreover, 53BP1 nuclear bodies, which co-localize with PML bodies, also occur within the nucleoli compartments. Irradiation of the human osteosarcoma cell line U2OS with γ-rays increases the degree of co-localization between 53BP1 and PML bodies throughout the genome; however, the 53BP1 protein is less abundant in chromatin of ribosomal genes and fragile sites (FRA3B and FRA16D) in γ-irradiated cells. Most epigenomic marks on ribosomal genes and fragile sites are relatively stable in both non-irradiated and γ-irradiated cells. However, H3K4me2, H3K9me3, H3K27me3 and H3K79me1 were significantly changed in promoter and coding regions of ribosomal genes after exposure of cells to γ-rays. In fragile sites, γ-irradiation induces a decrease in H3K4me3, changes the levels of HP1β, and modifies the levels of H3K9 acetylation, while the level of H3K9me3 was relatively stable. In these studies, we confirm a specific DNA-damage response that differs between the ribosomal genes and fragile sites, which indicates the region-specificity of DNA repair.