The discordance between genome size and the complexity of eukaryotes can partly be attributed to differences in repeat density. The Muller F element (∼5.2 Mb) is the smallest chromosome in Drosophila melanogaster, but it is substantially larger (>18.7 Mb) in D. ananassae. To identify the major contributors to the expansion of the F element and to assess their impact, we improved the genome sequence and annotated the genes in a 1.4-Mb region of the D. ananassae F element, and a 1.7-Mb region from the D element for comparison. We find that transposons (particularly LTR and LINE retrotransposons) are major contributors to this expansion (78.6%), while Wolbachia sequences integrated into the D. ananassae genome are minor contributors (0.02%). Both D. melanogaster and D. ananassae F-element genes exhibit distinct characteristics compared to D-element genes (e.g., larger coding spans, larger introns, more coding exons, and lower codon bias), but these differences are exaggerated in D. ananassae. Compared to D. melanogaster, the codon bias observed in D. ananassae F-element genes can primarily be attributed to mutational biases instead of selection. The 5′ ends of F-element genes in both species are enriched in dimethylation of lysine 4 on histone 3 (H3K4me2), while the coding spans are enriched in H3K9me2. Despite differences in repeat density and gene characteristics, D. ananassae F-element genes show a similar range of expression levels compared to genes in euchromatic domains. This study improves our understanding of how transposons can affect genome size and how genes can function within highly repetitive domains.

Histone acetylation is directly related to gene expression. In yeast, the acetyltransferase general control nonderepressible-5 (GCN5) targets histone H3 and associates with transcriptional co-activators alteration/deficiency in activation-2 (ADA2) and alteration/deficiency in activation-3 (ADA3) in complexes like SAGA. Arabidopsis thaliana has two genes encoding proteins, designated ADA3a and ADA3b, that correspond to yeast ADA3. We investigated the role of ADA3a and ADA3b in regulating gene expression during flowering time. Specifically, we found that knock out mutants ada3a-2 and the double mutant ada3a-2 ada3b-2 lead to early flowering compared to the wild type plants under long day (LD) conditions and after moving plants from short days to LD. Consistent with ADA3a being a repressor of floral initiation, FLOWERING LOCUS T (FT) expression was increased in ada3a mutants. In contrast, other genes involved in multiple pathways leading to floral transition, including FT repressors, players in GA signaling, and members of the SPL transcriptional factors, displayed reduced expression. Chromatin immunoprecipitation analysis revealed that ADA3a affects the histone H3K14 acetylation levels in SPL3, SPL5, RGA, GAI, and SMZ loci. In conclusion, ADA3a is involved in floral induction through a GCN5-containing complex that acetylates histone H3 in the chromatin of flowering related genes.

In an ever-changing environment, animals often need to switch between performing different tasks involving distinct sets of cognitive processes. Many such tasks involve neural activity distributed across the cortex, with dynamics that depend on both task demands and behavioral strategy. A fundamental but unanswered question is what circuit mechanisms orchestrate these task-dependent dynamics. Here, we hypothesized that acetylcholine release in the cortex plays a key role. The cortex's only long-range source of this neuromodulator is the basal forebrain cholinergic system, which targets the entire cortical sheet and can individually modulate single regions on sub-second timescales. To test our hypothesis, we first imaged cholinergic axons innervating the cortex while mice switched frequently between two navigational decision-making tasks in virtual reality (VR), only one of which required gradual accumulation of sensory evidence. We found that cholinergic input to the cortex is spatiotemporally heterogeneous and multiplexes sensory, motor, arousal, and cognitive signals in a task- and strategy-dependent fashion, with overall higher activity during evidence accumulation. Crucially, beyond contextual variables, cholinergic activity directly tracked task computations themselves, encoding an evidence-dependent decision variable only in the accumulation task. To test if acetylcholine release is causal to the performance of each task, we optogenetically silenced cholinergic terminals in the cortex while simultaneously imaging excitatory cortical activity. We found that this input is selectively required for evidence accumulation, and for large-scale cortical coding of evidence and choice during the accumulation task. Thus, we have identified a new cholinergic mechanism that orchestrates cortex-wide activity in a task-dependent manner and serves as a key node in the distributed brain network underlying the accumulation of sensory evidence.

We present a gene model for the ortholog of Glycogen phosphorylase ( Glyp ) in the D. ananassae May 2011 (Agencourt dana_caf1/DanaCAF1) genome assembly of Drosophila ananassae (GenBank Accession: GCA_000005115.1). This ortholog was characterized as part of a developing dataset to study the evolution of the insulin/insulin-like growth factor signaling pathway (IIS) across the genus Drosophila using the Genomics Education Partnership gene annotation protocol for Course-based Undergraduate Research Experiences.

This case aims to strengthen students’ understanding of molecular biology concepts through study of Fragile X Syndrome (FXS). Students begin by learning the cause and phenotypes of FXS and related conditions. Students then apply genetics knowledge to describe the inheritance of FXS. Knowledge of the central dogma of molecular biology helps students understand the impact of genetic and epigenetic changes on expression of the Fragile X mental retardation gene 1 and the impacts of the loss of the Fragile X Mental Retardation Protein on other protein production. As one example of the latter, students look at alterations in metabolic enzymes and consider ways to mitigate the phenotype, proposing treatments for FXS. Throughout the case, students are pointed to a clinical website and scientific literature to build their understanding. This case study also engages students in consideration of diversity and inclusion in conveying, interpreting, and acting on scientific information. Overall, this case can help students connect biological concepts to a real-world application while developing their abilities to think critically and comprehend scientific information. Primary Image: “Fragile X metaphase spread,” showing human chromosomes with the Fragile X site highlighted with an arrow. This image was accessed via Creative Commons and available under license CC BY 4.0 (provider Europeana, source Wellcome Collection).