By the end of this section, you will be able to:Understand how the cell cycle is controlled by mechanisms both internal and external to the cellExplain how the three internal control checkpoints occur at the end of G1, at the G2/M transition, and during metaphaseDescribe the molecules that control the cell cycle through positive and negative regulation

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:Understand how the cell cycle is controlled by mechanisms both internal and external to the cellExplain how the three internal control checkpoints occur at the end of G1, at the G2/M transition, and during metaphaseDescribe the molecules that control the cell cycle through positive and negative regulation

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:

"Apoptosis, a form of programmed cell death, plays critical roles in animal development and in repair of DNA damage. Since DNA damage is a major factor in cancer development, identifying the regulators of damage-induced apoptosis could help researchers develop treatments. A recent study investigated whether NHR-14, an important developmental protein in the model organism C. elegans, also contributes to damage-induced apoptosis . using mutant C. elegans that are especially susceptible to radiation-induced DNA damage. Deletion of the gene encoding NHR-14, which corresponds to HNF4 in humans, decreased radiation-induced apoptosis of sex cells without affecting the levels of normal (non-damage-induced) apoptosis, indicating a specific role in the damage-induced death pathway. Further exploration revealed that the NHR-14 gene acts “downstream” of the DNA damage checkpoint pathway and regulates the transcription of the genes egl-1 and ced-13 after DNA is damaged..."

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:

"p53 is widely considered the most frequently mutated gene in human disease, including in cancer. Normally, p53 acts as a checkpoint for recognizing DNA damage and actually suppresses tumor formation. Alterations to p53 compromise this function and can make way for life-threatening tumor growth. A new study examined how abnormal p53 might create conditions favorable for one of the most aggressive forms of ovarian carcinoma. The authors of the study began by knocking the p53 gene out of ovarian carcinoma cells and monitoring the effects. Next-generation sequencing of the p53-less cells revealed significantly elevated expression of fibronectin, a structural protein linked to various carcinomas. Loss of p53 function also appeared to boost the cancer cells’ ability to migrate and spread. Data on actual patients with ovarian cancer confirmed the pattern observed in the lab..."

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:

"Familial adenomatous polyposis (FAP) is an inherited disorder characterized by the formation of up to several thousand tumors in the rectum and colon. FAP is usually caused by a mutation of the adenomatous polyposis coli (APC) gene. While the molecular changes linking this mutation to tumor formation are not fully understood, dysregulated apoptosis—a form of programmed cell death—is known to play a prominent role. Now, researchers have uncovered a pattern of expression of an apoptosis-regulating protein that may help explain how FAP tumors form. The protein is called apoptosis repressor with caspase recruitment domain, or ARC. The team examined the expression of ARC in 212 FAP tumor samples from 80 patients. They found that ARC was expressed in the cytoplasm of most tumor cells, as well as in the nuclei..."

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:

"Breast cancer remains one of the most common cancers among women, indicating that better treatments are needed. The drug THZ1 is effective against triple-negative breast cancer, which frequently features overexpression-inducing mutations in the protein p53. However, THZ1 is ineffective against breast cancer cells with nonmutated (wild-type, WT) p53. To improve treatment options, researchers recently tried to increase the THZ1 sensitivity of WT p53 breast cancer cells. Treating the cells with nutlin-3, a molecule that indirectly prevents p53 degradation, enhanced the killing ability of THZ1, and overexpression experiments confirmed that this sensitization was due to upregulation of functional p53. Further investigation into the mechanism revealed that p53 accumulated in the nuclei and mitochondria of the dying cells after nutlin-3 and THZ1 treatment..."

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