A striking aspect of evolution is that it often converges on similar trajectories. Evolutionary convergence can occur in deep time or over short time scales, and is associated with the imposition of similar selective pressures. Repeated convergent events provide a framework to infer the genetic basis of adaptive traits. The current study examines the genetic basis of secondary web loss within web-building spiders (Araneoidea). Specifically, we use a lineage of spiders in the genus Tetragnatha (Tetragnathidae) that has diverged into two clades associated with the relatively recent (5mya) colonization of, and subsequent adaptive radiation within, the Hawaiian Islands. One clade has adopted a cursorial lifestyle, and the other has retained the ancestral behavior of capturing prey with sticky orb webs. We explore how these behavioral phenotypes are reflected in the morphology of the spinning apparatus and internal silk glands, and the expression of silk genes. Several sister families to the Tetragnathidae have egradation, and processing, which are processes that play important roles in silk production. This study demonstrates, in the case of independent evolution of web loss, that similar selective pressures act on many of the same genes to produce the same phenotypes and behaviors.
 Our results provide strong evidence that independent web loss events and the associated adoption of a cursorial lifestyle are based on similar genetic mechanisms. Many genes we identified as having evolved convergently are associated with protein synthesis, degradation, and processing, which are processes that play important roles in silk production. This study demonstrates, in the case of independent evolution of web loss, that similar selective pressures act on many of the same genes to produce the same phenotypes and behaviors.
  Cotton fiber is a model system for studying plant cell development. At present, the functions of many transcription factors in cotton fiber development have been elucidated, however, the roles of auxin response factor (ARF) genes in cotton fiber development need be further explored.
 
  Here, we identify auxin response factor (ARF) genes in three cotton species the tetraploid upland cotton G. hirsutum, which has 73 ARF genes, and its putative extent parental diploids G. arboreum and G. raimondii, which have 36 and 35 ARFs, respectively. Ka and Ks analyses revealed that in G. hirsutum ARF genes have undergone asymmetric evolution in the two subgenomes. The cotton ARFs can be classified into four phylogenetic clades and are actively expressed in young tissues. We demonstrate that GhARF2b, a homolog of the Arabidopsis AtARF2, was preferentially expressed in developing ovules and fibers. Overexpression of GhARF2b by a fiber specific promoter inhibited fiber cell elongation but promoted initiation and, conversely, its downregulation by RNAi resulted in fewer but longer fiber. We show that GhARF2b directly interacts with GhHOX3 and represses the transcriptional activity of GhHOX3 on target genes.
 
  Our results uncover an important role of the ARF factor in modulating cotton fiber development at the early stage.
 Our results uncover an important role of the ARF factor in modulating cotton fiber development at the early stage.
  Disorders of gene dosage can significantly increase risk for psychopathology, but outcomes vary greatly amongst carriers of any given chromosomal aneuploidy or sub-chromosomal copy number variation (CNV). One potential path to advance precision medicine for neurogenetic disorders is modeling penetrance in probands relative to observed phenotypes in their non-carrier relatives. Here, we seek to advance this general analytic framework by developing new methods in application to XYY syndrome-a sex chromosome aneuploidy that is known to increase risk for psychopathology.
 
  We analyzed a range of cognitive and behavioral domains in XYY probands and their non-carrier family members (n = 58 families), including general cognitive ability (FSIQ), as well as continuous measures of traits related to autism spectrum disorder (ASD) and attention deficit hyperactivity disorder (ADHD). Proband and relative scores were compared using covariance, regression and cluster analysis. Comparisons were made both within and across ry 01 October 1989.
 ClinicalTrials.gov NCT00001246 , "89-M-0006 Brain Imaging of Childhood Onset Psychiatric Disorders, Endocrine Disorders and Healthy Controls." Date of registry 01 October 1989.
  Tilapia (Oreochromis niloticus) cultures are frequently infected by Vibrio vulnificus, causing major economic losses to production units. Previously, tilapia expressing recombinant delta-5 desaturase and delta-6 desaturase (D56) were found to be resistant to V.  https://www.selleckchem.com/products/pd0166285.html  vulnificus infection. In this report, we profile the D56-mediated molecular changes underlying this resistance in tilapia. A comparative transcriptome analysis was performed on V. vulnificus-infected wild-type and D56-transgenic tilapia using Illumina's sequencing-by-synthesis approach. Gene enrichment analysis on differentially expressed unigenes was performed, and the expression patterns were validated by real-time PCR.
 
  Comparative transcriptome analysis was performed on RNA-sequence profiles obtained from wild-type and D56-transgenic tilapia at 0, 6 and 24 h post-infection with V. vulnificaus. GO and KEGG gene enrichment analyses showed that D56 regulates several pathways and genes, including fatty acid (FA) metabolism associated, and inflammatoansgenic tilapia to V. vulnificus.
 Transcriptome profiling and filtering for two-fold change variation showed that 3795 genes were upregulated and 1839 genes were downregulated in D56-transgenic tilapia. These genes were grouped into pathways, such as FA metabolism, FA elongation, FA biosynthesis, biosynthesis of unsaturated FA, FA degradation, inflammation, immune response, and chemokines. FA-associated genes and immune-related genes were modulated by D56 at 6 h and 24 h post infection with V. vulnificus. The expression patterns of FA-related genes, inflammatory genes, antimicrobial peptide genes and immune responsive genes at 0, 3, 6, 12, 24 and 48 h post-infection suggests these genes are involved in the enhanced resistance of D56 transgenic tilapia to V. vulnificus.