A thorough understanding of the molecular biosciences requires the ability to visualize and manipulate molecules in order to interpret results or to generate hypotheses. While many instructors in biochemistry and molecular biology use visual representations, few indicate that they explicitly teach visual literacy. One reason is the need for a list of core content and competencies to guide a more deliberate instruction in visual literacy. We offer here the second stage in the development of one such resource for biomolecular three‐dimensional visual literacy. We present this work with the goal of building a community for online resource development and use. In the first stage, overarching themes were identified and submitted to the biosciences community for comment: atomic geometry; alternate renderings; construction/annotation; het group recognition; molecular dynamics; molecular interactions; monomer recognition; symmetry/asymmetry recognition; structure‐function relationships; structural model skepticism; and topology and connectivity. Herein, the overarching themes have been expanded to include a 12th theme (macromolecular assemblies), 27 learning goals, and more than 200 corresponding objectives, many of which cut across multiple overarching themes. The learning goals and objectives offered here provide educators with a framework on which to map the use of molecular visualization in their classrooms. In addition, the framework may also be used by biochemistry and molecular biology educators to identify gaps in coverage and drive the creation of new activities to improve visual literacy. This work represents the first attempt, to our knowledge, to catalog a comprehensive list of explicit learning goals and objectives in visual literacy. © 2016 by The International Union of Biochemistry and Molecular Biology, 45(1):69–75, 2017.

Although several hundred genes are directly or indirectly regulated by steroid hormones, significant gaps exist in our understanding of the relevant mechanisms, particularly for those genes that do not directly bind intracellular receptors or that exhibit delayed changes in transcription rates upon receptor binding. To assist in defining the mechanism of action of steroid hormones, we are proposing that a standard nomenclature be adopted for classifying steroid-responsive genes, based upon whether the receptors directly bind to the target genes and the kinetics of the response. Three categories are proposed: primary response genes, delayed primary response genes, and secondary response genes.

Because induction of the chicken ovalbumin (Ov) gene by steroid hormones requires concomitant protein synthesis, efforts have focused on defining the binding site in the Ov gene for a labile transcription factor. Previous gel mobility shift studies identified one such site in the steroid-dependent regulatory element (SDRE) between ؊900 and ؊853. To ascertain whether estrogen and glucocorticoid affect the binding of this labile protein, genomic footprinting of the Ov gene was done by treating primary oviduct cell cultures with dimethyl sulfate. Several alterations that include steroid-dependent protection of guanine residues ؊889 and ؊885 and hypersensitivity of adenine residues ؊892 and ؊865 were observed. Of particular importance, the in vivo footprinting data are corroborated by two functional studies, one with linker-scanning mutations and the other with point mutations. Ten-base-pair linker-scanning mutations between ؊900 and ؊878 severely reduced the induction by estrogen and glucocorticoid. Likewise, point mutations of the protected guanine residues profoundly attenuated the response to these steroid hormones. In addition, in vitro binding activity correlated with in vivo functional activity. For example, mutant A4e shows no transcriptional activity in response to steroid hormones, and a corresponding oligomer does not bind protein in vitro. In contrast, mutant A4c is fully active in both contexts. These data support the contention that the ovalbumin gene is regulated by a steroid hormone-induced transcriptional cascade that culminates in the binding of chicken ovalbumin induced regulatory protein or protein complex (Chirp-I) to a DNA element from ؊891 to ؊878 in the SDRE.Eukaryotic genes are primarily regulated by the modulation of the initiation of transcription via the binding of proteins to DNA flanking the coding sequences of genes. Two basic models have been proposed to explain the effects that trans-acting proteins have on transcription rates when bound to their cisacting DNA elements (42). The first of these models involves altering the topology of the DNA by assembling a three-dimensional multimeric complex. The roles of several proteins that appear to be involved in rearranging chromatin structure are explained by this model. The second model invokes protein-protein interactions between the bound transcription factors and members of the general transcriptional machinery (42). These models are not mutually exclusive, and both rely on the ability of trans-acting factors to recognize a specific DNA element(s) in order to impart specificity to the response.Steroid receptors apparently affect the initiation of transcription through both of the mechanisms described above, chromatin remodeling (3) and direct protein-protein interaction (17). Steroid hormones activate transcription by binding to specific receptor proteins, which then bind to well-defined DNA sequences in specific steroid-regulated genes (21). The steroid receptor binding sites or steroid response elements (SREs) behave as true enhancers....

Although several hundred genes are directly or indirectly regulated by steroid hormones, significant gaps exist in our understanding of the relevant mechanisms, particularly for those genes that do not directly bind intracellular receptors or that exhibit delayed changes in transcription rates upon receptor binding. To assist in defining the mechanism of action of steroid hormones, we are proposing that a standard nomenclature be adopted for classifying steroid-responsive genes, based upon whether the receptors directly bind to the target genes and the kinetics of the response. Three categories are proposed: primary response genes, delayed primary response genes, and secondary response genes.

We have isolated and characterized lamb liver cDNAs encoding ovine insulin-like growth factor-I (oIGF-I) precursor polypeptide to study IGF-I gene expression in ruminants. Four cDNA clones were sequenced revealing two different exon 1 sequences (designated 1A and 1B) and four different putative poly(A) adenylation sites. cDNAs containing exon 1A or exon 1B encode precursor polypeptides of 138 or 154 amino acids, respectively. A 130-amino-acid peptide is encoded by all cDNAs examined. These precursors include a hydrophobic leader peptide of varying lengths, the 70-amino-acid oIGF-I, and a 35-amino-acid carboxyl terminal extension peptide. The predicted amino acid sequence of the oIGF-I peptide differs from the human, bovine, and porcine IGF-Is at a single amino acid (at position 66, alanine is substituted for proline) and differs from rat and mouse IGF-Is at 4 and 5 positions, respectively. Both the amino- and carboxy-terminal extension peptides showed regions of extensive sequence homology. Ovine IGF-I amino-terminal peptides are 1 amino acid longer than other mammalian IGFs due to the presence of an extra amino acid (glutamine) present at the proposed boundary of exon 1 and exon 2. Northern blot analysis revealed multiple oIGF-I transcripts in a broad band at 800-1,100 nucleotides and other transcripts of higher molecular weight in liver. There was no detectable expression in either spleen or brain.