Ankfn1-mutant vestibular defects require loss of both ancestral and derived paralogs for penetrance in zebrafish

How and to what degree gene duplication events create regulatory innovation, redundancy, or neofunctionalization remain important questions in animal evolution and comparative genetics. Ankfn1 genes are single copy in most invertebrates, partially duplicated in jawed vertebrates, and only the derived copy retained in most mammals. Null mutations in the single mouse homolog have vestibular and neurological abnormalities. Null mutation of the single Drosophila homolog is typically lethal with severe sensorimotor deficits in rare survivors. The functions and potential redundancy of paralogs in species with two copies is not known. Here we define a vestibular role for Ankfn1 homologs in zebrafish based on simultaneous disruption of each locus. Zebrafish with both paralogs disrupted showed vestibular defects and early lethality from swim bladder inflation failure. One intact copy at either locus was sufficient to prevent major phenotypes. Our results show that vertebrate Ankfn1 genes are required for vestibular-related functions, with at least partial redundancy between ancestral and derived paralogs.

Ankfn1 vestibular defects in zebrafish require mutations in both ancestral and derived paralogs.

How and to what degree gene duplication events create regulatory innovation, redundancy, or neofunctionalization remain important questions in animal evolution and comparative genetics. Ankfn1 genes are single copy in most invertebrates, partially duplicated in jawed vertebrates, and only the derived copy retained in most mammals. Null mutations in the single mouse homolog have vestibular and neurological abnormalities. Null mutation of the single Drosophila homolog is typically lethal with severe sensorimotor deficits in rare survivors. The functions and potential redundancy of paralogs in species with two copies is not known. Here we define a vestibular role for Ankfn1 homologs in zebrafish based on simultaneous disruption of each locus. Zebrafish with both paralogs disrupted showed vestibular defects and early lethality from swim bladder inflation failure. One intact copy at either locus was sufficient to prevent major phenotypes. Our results show that vertebrate Ankfn1 genes are required for vestibular-related functions, with at least partial redundancy between ancestral and derived paralogs.

The information signature of diverging lineages

The process of forming new species is the driving force behind the diversity of life on Earth. Yet, we have not answered the basic question: why are species unevenly distributed across taxonomic groups and geographic settings? This is because we lack the means to directly compare aspects of population (lineage) divergence across unrelated species because taxon-specific effects make comparisons difficult or impossible. Here, we present a new solution to this challenge by identifying the information signature of diverging lineages, calculated using partial information decomposition (PID), under different evolutionary scenarios. We show in silico how the informational decomposition of genetic metrics varies over time since divergence. Calculating PID over 97,200 lattices reveals that the decomposed nodes of Tajima’s D, θW, and π have strong information signatures, while FST was least useful for discriminating among divergence scenarios. The presence or absence of gene flow during divergence was the most detectable signature; mutation rate and effective population size (Ne) were also detectable whereas differences in recombination rate were not. This work demonstrates that PID can reveal evolutionary patterns that are minimally detectable using the raw metrics themselves; it does so by leveraging the architecture of the genome and the partial redundancy of information contained in genetic metrics. Our results demonstrate for the first time how to directly compare characteristics of diverging populations even among distantly related species, providing a foundational tool for understanding the diversity of life across Earth.

Spatial and temporal variation and the influence of environmental parameters in a fish community in the Una River, Paraíba do Sul Valley, São Paulo

Understanding of aspects of the structure of ichthyological communities and how these relate to the environment and its natural variation has been one of the principal objectives of ecological studies conducted in freshwater environments. The objective of this study was to evaluate the relationship between fish species composition in the Una River and environmental variables during dry and rainy seasons. Data collection was done along three stretches of the main channel of the Una River between April 2016 and March 2017. In general, the riverbed presented a high degree of silting in all study sites. A total of 1,534 fish specimens from thirty species were collected. There was greater richness and abundance of species during the rainy season in all sampled areas. A Partial Redundancy Analysis (pRDA) showed a significant correlation between the fish community, substrate composition, and concentrations of dissolved oxygen in the water. The qualitative structure of the ichthyofauna indicated a greater association with environmental structure than with seasonality, since there was a clear tendency for the three stretches of river to group together independent of the sampling period. There were no significant differences between the indices of diversity registered for the dry and rainy seasons. This is due to the dominance of the species Astyanax aff. bimaculatus (two spot Astyanax | lambari-do-rabo-amarelo) and Hypostomus cf. luetkeni (armoured catfish | cascudo), which represented more than half of the collected specimens during the rainy season.

Genetic evidence for partial redundancy between the arginine methyltransferases CARM1 and PRMT6

CARM1 is a protein arginine methyltransferase (PRMT) that acts as a coactivator in a number of transcriptional programs. CARM1 orchestrates this coactivator activity in part by depositing the H3R17me2a histone mark in the vicinity of gene promoters that it regulates. However, the gross levels of H3R17me2a in CARM1 KO mice did not significantly decrease, indicating that other PRMT(s) may compensate for this loss. We thus performed a screen of type I PRMTs, which revealed that PRMT6 can also deposit the H3R17me2a mark in vitro. CARM1 knockout mice are perinatally lethal and display a reduced fetal size, whereas PRMT6 null mice are viable, which permits the generation of double knockouts. Embryos that are null for both CARM1 and PRMT6 are noticeably smaller than CARM1 null embryos, providing in vivo evidence of redundancy. Mouse embryonic fibroblasts (MEFs) from the double knockout embryos display an absence of the H3R17me2a mark during mitosis and increased signs of DNA damage. Moreover, using the combination of CARM1 and PRMT6 inhibitors suppresses the cell proliferation of WT MEFs, suggesting a synergistic effect between CARM1 and PRMT6 inhibitions. These studies provide direct evidence that PRMT6 also deposits the H3R17me2a mark and acts redundantly with CARM1.

Mosquito Community Composition, Seasonal Distributions, and Trap Bias in Northeastern Florida

Mosquito control agencies monitor mosquito diversity and abundance through a variety of trap types. Although various long-term ecological data sets exist, little work has been done to address the sampling effort required to capture mosquito community diversity by trap type and few spatiotemporal distributions of vector species have been described. Here, we describe the seasonal distributions of vector species of importance, assess trapping effort needed to capture the diversity of the mosquito community, and use a partial redundancy analysis to identify trap bias from four commonly deployed adult mosquito traps in Volusia County, Florida. Collections were made with American Biophysics Corporation (ABC) light traps, Biogents Sentinel (BGS) traps, chicken coop exit traps, and gravid traps. We collected a total of 238,301 adult female mosquitoes belonging to 11 genera and 36 species, 12 of which we deemed to be vector species of epidemiological importance. We found that ABC traps not only yielded the greatest abundance and diversity but also captured several nonvector species. BGS and gravid traps yielded the highest proportions of vector species; exit traps recorded the lowest abundances and species richness. Wintertime abundances of several species demonstrated a need for year-round surveillance in the study area; partial redundancy analysis revealed that trap type explained a significant proportion of the variance in our data set, with certain vector species associated with specific trap types. Increased awareness regarding the amount of trapping effort needed to detect vector species diversity will help to optimize efforts in the field, leading to more effective resource allocation.

Ubiquitin receptors are required for substrate-mediated activation of the proteasome’s unfolding ability

The ubiquitin-proteasome system (UPS) is responsible for the bulk of protein degradation in eukaryotic cells, but the factors that cause different substrates to be unfolded and degraded to different extents are still poorly understood. We previously showed that polyubiquitinated substrates were degraded with greater processivity (with a higher tendency to be unfolded and degraded than released) than ubiquitin-independent substrates. Thus, even though ubiquitin chains are removed before unfolding and degradation occur, they affect the unfolding of a protein domain. How do ubiquitin chains activate the proteasome’s unfolding ability? We investigated the roles of the three intrinsic proteasomal ubiquitin receptors - Rpn1, Rpn10 and Rpn13 - in this activation. We find that these receptors are required for substrate-mediated activation of the proteasome’s unfolding ability. Rpn13 plays the largest role, but there is also partial redundancy between receptors. The architecture of substrate ubiquitination determines which receptors are needed for maximal unfolding ability, and, in some cases, simultaneous engagement of ubiquitin by multiple receptors may be required. Our results suggest physical models for how ubiquitin receptors communicate with the proteasomal motor proteins.

Ubiquitin receptors are required for substrate-mediated activation of the proteasome’s unfolding ability

ABSTRACTThe ubiquitin-proteasome system (UPS) is responsible for the bulk of protein degradation in eukaryotic cells, but the factors that cause different substrates to be unfolded and degraded to different extents are still poorly understood. We previously showed that polyubiquitinated substrates were degraded with greater processivity (with a higher tendency to be unfolded and degraded than released) than ubiquitin-independent substrates. Thus, even though ubiquitin chains are removed before unfolding and degradation occur, they affect the unfolding of a protein domain. How do ubiquitin chains activate the proteasome’s unfolding ability? We investigated the roles of the three intrinsic proteasomal ubiquitin receptors - Rpn1, Rpn10 and Rpn13 - in this activation. We find that these receptors are required for substrate-mediated activation of the proteasome’s unfolding ability. Rpn13 plays the largest role, but there is also partial redundancy between receptors. The architecture of substrate ubiquitination determines which receptors are needed for maximal unfolding ability, and, in some cases, simultaneous engagement of ubiquitin by multiple receptors may be required. Our results suggest physical models for how ubiquitin receptors communicate with the proteasomal motor proteins.