bims-sevkro 2018-07-15 papers

Genome Biol Evol. 2018 Jul 05.

Whole genome sequencing of the Pirarucu (Arapaima gigas) supports independent emergence of major teleost clades.

Ricardo Assunção Vialle, Jorge Estefano Santana de Souza, Katia de Paiva Lopes, Diego Gomes Teixeira, Pitágoras de Azevedo Alves Sobrinho, André M Ribeiro-Dos-Santos, Carolina Furtado, Tetsu Sakamoto, Fábio Augusto Oliveira Silva, Edivaldo Herculano Corrêa de Oliveira, Igor Guerreiro Hamoy, Paulo Pimentel Assumpção, Ândrea Ribeiro-Dos-Santos, João Paulo Matos Santos Lima, Héctor N Seuánez, Sandro José de Souza, Sidney Santos.

The Pirarucu (Arapaima gigas) is one of the world's largest freshwater fishes and member of the superorder Osteoglossomorpha (bonytongues), one of the oldest lineages of ray-finned fishes. This species is an obligate air-breather found in the basin of the Amazon River with an attractive potential for aquaculture. Its phylogenetic position among bony fishes makes the Pirarucu a relevant subject for evolutionary studies of early teleost diversification. Here, we present, for the first time, a draft genome version of the A. gigas genome, providing useful information for further functional and evolutionary studies. The A. gigas genome was assembled with 103 Gb raw reads sequenced in an Illumina platform. The final draft genome assembly was approximately 661 Mb, with a contig N50 equal to 51.23 kb and scaffold N50 of 668 kb. Repeat sequences accounted for 21.69% of the whole genome, and a total of 24,655 protein-coding genes were predicted from the genome assembly, with an average of 9 exons per gene. Phylogenomic analysis based on 24 fish species supported the postulation that Osteoglossomorpha and Elopomorpha (eels, tarpons and bonefishes) are sister groups, both forming a sister lineage with respect to Clupeocephala (remaining teleosts). Divergence time estimations suggested that Osteoglossomorpha and Elopomorpha lineages emerged independently in a period of approximately 30 million years in the Jurassic. The draft genome of A. gigas provides a valuable genetic resource for further investigations of evolutionary studies and may also offer a valuable data for economic applications.

DOI: https://doi.org/10.1093/gbe/evy130

Integr Comp Biol. 2018 Jul 05.

'The same thing that makes you live can kill you in the end': exploring the effects of growth rates and longevity on cellular metabolic rates and oxidative stress in mammals and birds.

Ana Gabriela Jimenez.

All aerobic organisms are subjected to metabolic by-products known as reactive species (RS).RS can wreak havoc on macromolecules by structurally altering proteins and inducing mutations in DNA, among other deleterious effects. . To combat accumulating damage, organisms have an antioxidant system to sequester RS before they cause cellular damage. The balance between RS production, antioxidant defences, and accumulated cellular damage is termed oxidative stress. Physiological ecologists, gerontologists and metabolic biochemists have turned their attention to whether oxidative stress is the principal, generalized mechanism that mediates and limits longevity, growth rates and other life-history trade-offs in animals, as may be the case in mammals and birds. At the crux of this theory lies the regulation and activities of the mitochondria with respect to the organism and its metabolic rate. At the whole-animal level, evolutionary theory suggests that developmental trajectories and growth rates can shape the onset and rate of aging. Mitochondrial function is important for aging since it is the main source of energy in cells, and the main source of RS. Altering oxidative stress levels, either increases in oxidative damage or reduction in antioxidants, has proven to also decrease growth rates, which implies that oxidative stress is a cost of, as well as a constraint on, growth. Yet, in nature, many animals exhibit fast growth rates that lead to higher loads of oxidative stress, which are often linked to shorter lifespans. In this paper, I summarize the latest findings on whole-animal life history trade-offs, such as growth rates and longevity, and how these can be affected by mitochondrial cellular metabolism, and oxidative stress.

DOI: https://doi.org/10.1093/icb/icy090

Nucleic Acids Res. 2018 Jun 30.

Histone H1 acetylation at lysine 85 regulates chromatin condensation and genome stability upon DNA damage.

Yinglu Li, Zhiming Li, Liping Dong, Ming Tang, Ping Zhang, Chaohua Zhang, Ziyang Cao, Qian Zhu, Yongcan Chen, Hui Wang, Tianzhuo Wang, Danyu Lv, Lina Wang, Ying Zhao, Yang Yang, Haiying Wang, Hongquan Zhang, Robert G Roeder, Wei-Guo Zhu.

Linker histone H1 has a key role in maintaining higher order chromatin structure and genome stability, but how H1 functions in these processes is elusive. Here, we report that acetylation of lysine 85 (K85) within the H1 globular domain is a critical post-translational modification that regulates chromatin organization. H1K85 is dynamically acetylated by the acetyltransferase PCAF in response to DNA damage, and this effect is counterbalanced by the histone deacetylase HDAC1. Notably, an acetylation-mimic mutation of H1K85 (H1K85Q) alters H1 binding to the nucleosome and leads to condensed chromatin as a result of increased H1 binding to core histones. In addition, H1K85 acetylation promotes heterochromatin protein 1 (HP1) recruitment to facilitate chromatin compaction. Consequently, H1K85 mutation leads to genomic instability and decreased cell survival upon DNA damage. Together, our data suggest a novel model whereby H1K85 acetylation regulates chromatin structure and preserves chromosome integrity upon DNA damage.

DOI: https://doi.org/10.1093/nar/gky568