Biology is designed for multi-semester biology courses for science majors. It is grounded on an evolutionary basis and includes exciting features that highlight careers in the biological sciences and everyday applications of the concepts at hand. To meet the needs of today’s instructors and students, some content has been strategically condensed while maintaining the overall scope and coverage of traditional texts for this course. Instructors can customize the book, adapting it to the approach that works best in their classroom. Biology also includes an innovative art program that incorporates critical thinking and clicker questions to help students understand—and apply—key concepts.

By the end of this section, you will be able to:Describe the cytoskeletonCompare the roles of microfilaments, intermediate filaments, and microtubulesCompare and contrast cilia and flagellaSummarize the differences among the components of prokaryotic cells, animal cells, and plant cells

This illustrate the flagellum of a eukaryotic cell. The axoneme comprise the bulk of the flagellum and is composed of microtubules arranged in a 9 + 2 configuration. It also contains motor proteins and other components not shown.

This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:

"Glioblastoma (GBM), an aggressive cancer in the brain or spinal cord, is a devastating diagnosis. Although therapies exist, GBM has a poor prognosis, with a median survival of only 14-15 months after diagnosis. Key to its aggressiveness is the degree to which migrating GBM cells infiltrate adjacent brain tissue. GBM cells express the protein MACC1, which is a marker of metastasis and tumor cell migration. Unfortunately, how GBM cells learn to migrate is unclear. A recent study used live-cell and atomic force microscopy to evaluate cell migration and mechanical properties of GBM cells overexpressing MACC1. The results showed that MACC1 increased the migratory speed and elasticity of GBM cells while it decreased cell-cell adhesion and inhibited aggregation. MACC1-overexpressing cells also had specific increases in protrusive actin, allowing the cells to adhere to laminin..."

The rest of the transcript, along with a link to the research itself, is available on the resource itself.

This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:

"Alzheimer’s disease and similar neurodegenerative diseases involve aggregation of the protein Tau and disruption of cell structural networks. The protein HDAC6 helps clear Tau aggregates and regulate the cytoskeleton, thus exerting neuroprotective effects. HDAC6’s catalytic domains mediate some of these functions, but the roles of another domain, the zinc finger ubiquitin-binding domain (ZnF UBP), are less understood. A recent study investigated the effects of purified HDAC6 ZnF UBP on cultured neuronal cells. The researchers found that HDAC6 ZnF UBP was nontoxic to cells, and cell imaging showed that it promoted reorganization of the cytoskeletal components actin and tubulin in ways that likely support neuron growth and migration. Localization of the protein ApoE in cell nuclei was increased, indicating improved neuronal health..."

The rest of the transcript, along with a link to the research itself, is available on the resource itself.

This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:

"Normally bound to the microtubules that give neurons their structure, the protein tau becomes detached in the brains of patients with Alzheimer’s disease. That leads to the fibrillary tangles that have become the hallmark of the disease. Most textbooks explain that post-translational modifications, or PTMs, in the form of excessive phosphorylation trigger the formation and growth of these bundles. But new findings propose a subtle though crucial refinement. Researchers from the Brain Mind Institute at the EPFL in Switzerland have discovered that while phosphorylation does trigger tau detachment, it doesn’t appear to promote tangle growth. It actually protects against it. Their findings offer a new perspective on the role of phosphorylation in tau pathologies, while encouraging the design of therapeutics that target tau detachment. Numerous studies have homed in on hyperphosphorylation as a trigger for tau pathologies. Unfortunately, they’ve done so with relatively poor resolution..."

The rest of the transcript, along with a link to the research itself, is available on the resource itself.