Sequencing and Characterization of the Invasive Sycamore Lace Bug <i>Corythucha ciliata</i> (Hemiptera: Tingidae) Transcriptome

<div><p>The sycamore lace bug, <i>Corythucha ciliata</i> (Hemiptera: Tingidae), is an invasive forestry pest rapidly expanding in many countries. This pest poses a considerable threat to the urban forestry ecosystem, especially to <i>Platanus</i> spp. However, its molecular biology and biochemistry are poorly understood. This study reports the first <i>C</i>. <i>ciliata</i> transcriptome, encompassing three different life stages (Nymphs, adults female (AF) and adults male (AM)). In total, 26.53 GB of clean data and 60,879 unigenes were obtained from three RNA-seq libraries. These unigenes were annotated and classified by Nr (NCBI non-redundant protein sequences), Nt (NCBI non-redundant nucleotide sequences), Pfam (Protein family), KOG/COG (Clusters of Orthologous Groups of proteins), Swiss-Prot (A manually annotated and reviewed protein sequence database), and KO (KEGG Ortholog database). After all pairwise comparisons between these three different samples, a large number of differentially expressed genes were revealed. The dramatic differences in global gene expression profiles were found between distinct life stages (nymphs and AF, nymphs and AM) and sex difference (AF and AM), with some of the significantly differentially expressed genes (DEGs) being related to metamorphosis, digestion, immune and sex difference. The different express of unigenes were validated through quantitative Real-Time PCR (qRT-PCR) for 16 randomly selected unigenes. In addition, 17,462 potential simple sequence repeat molecular markers were identified in these transcriptome resources. These comprehensive <i>C</i>. <i>ciliata</i> transcriptomic information can be utilized to promote the development of environmentally friendly methodologies to disrupt the processes of metamorphosis, digestion, immune and sex differences.</p></div

Summary of functional annotations of <i>C</i>. <i>Ciliata</i> unigenes.

<p>Summary of functional annotations of <i>C</i>. <i>Ciliata</i> unigenes.</p

Frequency of SSRs in <i>C</i>. <i>Ciliata</i> transcriptomes.

<p>Frequency of SSRs in <i>C</i>. <i>Ciliata</i> transcriptomes.</p

Coding sequence predictions of <i>C</i>. <i>Ciliata</i> transcriptome by BLASTx and ESTScan.

<p>(<b>a</b>) Length distribution of CDs using BLASTx (E-value < 10⁻⁵); (<b>b</b>) Length distribution of proteins using BLASTx; (<b>c</b>) Length distribution of CDs predicted by ESTScan, and <b>(d</b>) Length distribution of proteins using ESTScan.</p

Output statistics from AM, AF and Nymphs of <i>C</i>. <i>Ciliata</i>.

<p>Output statistics from AM, AF and Nymphs of <i>C</i>. <i>Ciliata</i>.</p

Volcano plots of differentially expressed unigenes.

<p>The abscissa represents the expressed levels fold change of unigenes in three different samples. The ordinate indicates the statistically significant difference degree. The lower and higher -log10 (p-adj) values mean greater differences. The scatters in diagram stand for each gene, the blue dot represents there was no significant difference of genes. The up-regulated and down-regulated genes were indicated by a red dot and green dot, respectively.</p

KEGG annotation of <i>C</i>. <i>Ciliata</i> predicted proteins.

<p>KEGG annotation of <i>C</i>. <i>Ciliata</i> predicted proteins.</p

Metamorphosis, digestion and immune related genes detected in the <i>C</i>. <i>Ciliata</i> DEGs dataset.

<p>Metamorphosis, digestion and immune related genes detected in the <i>C</i>. <i>Ciliata</i> DEGs dataset.</p

Pie charts showing distribution of the BLASTxmatches of <i>C</i>. <i>Ciliata</i> transcriptome unigenes against Nr databases.

<p>(a) E-values distribution, (b) similarity distribution, and (c) species classification.</p

Image_3_Sevoflurane exposure induces neurotoxicity by regulating mitochondrial function of microglia due to NAD insufficiency.JPEG

Developmental neurons received with sevoflurane, the commonly used inhalational anesthetic agent in clinical surgery, several times tend to be destroyed. Microglia, the resident immune cells of the central nervous system (CNS), are activated after sevoflurane exposure, accompanied by releasing proinflammatory cytokines that damage developing neurons. The sevoflurane-induced neurotoxicity could be attributed to activated microglia presenting proinflammatory and anti-inflammatory functions. Proinflammatory microglia release cytokines to impair the CNS, while anti-inflammatory microglia engulf damaged neurons to maintain CNS homeostasis. Sevoflurane exposure promotes the secretion of proinflammatory cytokines by microglia, inhibiting the microglial phagocytic function. Microglia with poor phagocytic function cannot engulf damaged neurons, leading to the accumulation of damaged neurons. The mechanism underlying poor phagocytic function may be attributed to mitochondrial dysfunction of microglia induced by sevoflurane exposure, in which affected mitochondria cannot generate adequate ATP and NAD to satisfy the energy demand. We discovered that sevoflurane treatment impaired the mitochondrial metabolism of microglia, which resulted in NAD deficiency and couldn’t produce sufficient energy to clear damaged neurons to maintain CNS development. Our findings provide an explanation of a new mechanism underlying sevoflurane-induced neurotoxicity.</p