Dataset Information

Rapidly evolving genetic features for desert adaptations in Stipagrostis pennata

ABSTRACT:

Background

Stipagrostis pennata is distributed in the mobile and semi-mobile sand dunes which can adapt well to extreme environments such as drought and high temperature. It is a pioneer plant species with potential for stabilizing sand dunes and ecological restoration. It can settle on moving sand dunes earlier than other desert plants. It can effectively improve the stability of sand dunes and help more plants settle down and increase plant diversity. However, despite its important ecological value, the genetic resources available for this species are limited.

Results

We used single-molecule real-time sequencing technology to obtain the complete full-length transcriptome of Stipagrostis pennata, including 90,204 unigenes with an average length of 2624 bp. In addition, the 5436 transcription factors identified in these unigenes are rich in stress resistance genes, such as MYB-related, C3H, bHLH, GRAS and HSF, etc., which may play a role in adapting to desert drought and strong wind stress. Intron retention events are abundant alternative splicing events. Stipagrostis pennata has experienced stronger positive selection, accelerating the fixation of advantageous variants. Thirty-eight genes, such as CPP/TSO1-like gene, have evolved rapidly and may play a role in material transportation, flowering and seed formation.

Conclusions

The present study captures the complete full-length transcriptome of Stipagrostis pennata and reveals its rapid evolution. The desert adaptation in Stipagrostis pennata is reflected in the regulation of gene expression and the adaptability of gene function. Our findings provide a wealth of knowledge for the evolutionary adaptability of desert grass species.

Supplementary Information

The online version contains supplementary material available at 10.1186/s12864-021-08124-w.

SUBMITTER: Ding X

PROVIDER: S-EPMC8609760 | biostudies-literature |

REPOSITORIES: biostudies-literature

ACCESS DATA

Similar Datasets

Project description:Pathogen adaptations during host-pathogen co-evolution can cause the host balance between immunity and immunopathology to rapidly shift. However, little is known in natural disease systems about the immunological pathways optimised through the trade-off between immunity and self-damage. The evolutionary interaction between the conjunctival bacterial infection Mycoplasma gallisepticum (MG) and its avian host, the house finch (Haemorhous mexicanus), can provide insights into such adaptations in immune regulation. Here we use experimental infections to reveal immune variation in conjunctival tissue for house finches captured from four distinct populations differing in the length of their co-evolutionary histories with MG and their disease tolerance (defined as disease severity per pathogen load) in controlled infection studies. To differentiate contributions of host versus pathogen evolution, we compared house finch responses to one of two MG isolates: the original VA1994 isolate and a more evolutionarily derived one, VA2013. To identify differential gene expression involved in initiation of the immune response to MG, we performed 3'-end transcriptomic sequencing (QuantSeq) of samples from the infection site, conjunctiva, collected 3-days post-infection. In response to MG, we observed an increase in general pro-inflammatory signalling, as well as T-cell activation and IL17 pathway differentiation, associated with a decrease in the IL12/IL23 pathway signalling. The immune response was stronger in response to the evolutionarily derived MG isolate compared to the original one, consistent with known increases in MG virulence over time. The host populations differed namely in pre-activation immune gene expression, suggesting population-specific adaptations. Compared to other populations, finches from Virginia, which have the longest co-evolutionary history with MG, showed significantly higher expression of anti-inflammatory genes and Th1 mediators. This may explain the evolution of disease tolerance to MG infection in VA birds. We also show a potential modulating role of BCL10, a positive B- and T-cell regulator activating the NFKB signalling. Our results illuminate potential mechanisms of house finch adaptation to MG-induced immunopathology, contributing to understanding of the host evolutionary responses to pathogen-driven shifts in immunity-immunopathology trade-offs.