Publications by authors named "Laura A Diaz-Martinez"

Article Synopsis
  • Biomedicine is moving towards decentralized data collection, which improves reproducibility and collaboration across labs.
  • A study evaluated biocytometry, a method using engineered bioparticles, and found it effective for counting target cells at low concentrations, even with varying user expertise.
  • The findings suggest that biocytometry is a practical option for immunophenotyping, allowing for sensitive and scalable analysis of rare cells in diverse samples without needing advanced training.
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Course-based undergraduate research experiences (CUREs) are increasingly becoming the first, and perhaps only, research experience for many biology students. Responsible and ethical conduct of research (RECR) is crucial for the integrity of scientific research and essential for students to have an understanding of the scientific process at any academic level. However, there is a current lack of RECR education in biology CUREs.

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Most studies on the benefits of participation in undergraduate research (UGR) use data from student participants in undergraduate research programs (URPs), which offer a limited number of positions. In reality, however, the majority of UGR students participate in undergraduate research not in programs (URNPs). The authors conducted an institution-wide study at a Hispanic-serving institution to examine the relationship between academic success and participation in these two UGR modalities.

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Course-based undergraduate research experiences (CUREs), which often engage students as early as freshman year, have become increasingly common in biology curricula. While many studies have highlighted the benefits of CUREs, little attention has been paid to responsible and ethical conduct of research (RECR) education in such contexts. Given this observation, we adopted a mixed methods approach to explore the extent to which RECR education is being implemented and assessed in biological sciences CUREs nationwide.

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Article Synopsis
  • Cohesin is a protein complex important for 3D genome organization, sister chromatid cohesion, and DNA repair but its ubiquitination mechanisms are not well understood.
  • Researchers used gene editing to tag cohesin components in human cells and identified the USP13 deubiquitinase as a key interacting protein with cohesin.
  • USP13 is essential for regulating cohesin's ubiquitination and its interaction with chromatin during cell division, though it does not affect sister chromatid cohesion directly.
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Advancement of the scientific enterprise relies on individuals conducting research in an ethical and responsible manner. Educating emergent scholars in the principles of ethics/responsible conduct of research (E/RCR) is therefore critical to ensuring such advancement. The recent impetus to include authentic research opportunities as part of the undergraduate curriculum, via course-based undergraduate research experiences (CUREs), has been shown to increase cognitive and noncognitive student outcomes.

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Course-based undergraduate research experiences (CUREs) have been identified as a promising vehicle to broaden novices' participation in authentic scientific opportunities. While recent studies in the bioeducation literature have focused on the influence of CUREs on cognitive and non-cognitive student outcomes (e.g.

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Genome stability is ensured by multiple surveillance mechanisms that monitor the duplication, segregation, and integrity of the genome throughout the cell cycle. Depletion of components of the spliceosome, a macromolecular machine essential for mRNA maturation and gene expression, has been associated with increased DNA damage and cell cycle defects. However, the specific role for the spliceosome in these processes has remained elusive, as different cell cycle defects have been reported depending on the specific spliceosome subunit depleted.

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The anticancer drug taxol stabilizes microtubules and activates the spindle checkpoint, causing prolonged mitotic arrest in cancer cells. Our recent work suggests that the cellular decision to live or die following mitotic arrest is a complex process involving crosstalk between competing apoptotic and adaptation pathways.

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The spindle checkpoint ensures accurate chromosome segregation by monitoring kinetochore-microtubule attachment. Unattached or tensionless kinetochores activate the checkpoint and enhance the production of the mitotic checkpoint complex (MCC) consisting of BubR1, Bub3, Mad2, and Cdc20. MCC is a critical checkpoint inhibitor of the anaphase-promoting complex/cyclosome, a ubiquitin ligase required for anaphase onset.

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The antimitotic anti-cancer drugs, including taxol, perturb spindle dynamics, and induce prolonged, spindle checkpoint-dependent mitotic arrest in cancer cells. These cells then either undergo apoptosis triggered by the intrinsic mitochondrial pathway or exit mitosis without proper cell division in an adaptation pathway. Using a genome-wide small interfering RNA (siRNA) screen in taxol-treated HeLa cells, we systematically identify components of the mitotic apoptosis and adaptation pathways.

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Most cancer cells are characterized by aneuploidy, an abnormal number of chromosomes. We have identified a clue to the mechanistic origins of aneuploidy through integrative genomic analyses of human tumors. A diverse range of tumor types were found to harbor deletions or inactivating mutations of STAG2, a gene encoding a subunit of the cohesin complex, which regulates the separation of sister chromatids during cell division.

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Multi-polar mitosis is strongly linked with aggressive cancers and it is a histological diagnostic of tumor-grade. However, factors that cause chromosomes to segregate to more than two spindle poles are not well understood. Here we show that cohesins Rad21, Smc1 and Smc3 are required for bipolar mitosis in human cells.

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Cohesin proteins help maintain the physical associations between sister chromatids that arise in S-phase and are removed in anaphase. Recent studies found that cohesins also localize to the centrosomes, the organelles that organize the mitotic bipolar spindle. We find that the cohesin protein Rad21 localizes to centrosomes in a manner that is dependent upon known regulators of sister chromatid cohesion as well as regulators of centrosome function.

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Classically, chromosomal functions in DNA repair and sister chromatid association have been assigned to the cohesin proteins. More recent studies have provided evidence that cohesins also localize to the centrosomes, which organize the bipolar spindle during mitosis. Depletion of cohesin proteins is associated with multi-polar mitosis in which spindle pole integrity is compromised.

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Long thought to be the glue responsible for holding sister chromatids together, cohesin has been found to be stickier than previously thought. Recent discoveries point to cohesin having a role in transcription regulation by mediating long-distance intra-chromosomal interactions.

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Accurate chromosome segregation constitutes the basis of inheritance. Mistakes in chromosome segregation during mitosis lead to aneuploidy, a common feature of tumors. The accuracy of chromosome segregation is governed by a complex network of processes which ensure that each daughter cell receives the correct number of chromosomes.

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Shugoshin 1 (Sgo1) protects centromeric sister-chromatid cohesion in early mitosis and, thus, prevents premature sister-chromatid separation. The protein level of Sgo1 is regulated during the cell cycle; it peaks in mitosis and is down-regulated in G1/S. Here we show that Sgo1 is degraded during the exit from mitosis, and its degradation depends on the anaphase-promoting complex/cyclosome (APC/C).

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Sister-chromatid cohesion is essential for accurate chromosome segregation. A key discovery towards our understanding of sister-chromatid cohesion was made 10 years ago with the identification of cohesins. Since then, cohesins have been shown to be involved in cohesion in numerous organisms, from yeast to mammals.

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During mitosis, the genome duplicated during S-phase is synchronously and accurately segregated to the two daughter cells. The spindle checkpoint prevents premature sister-chromatid separation and mitotic exit. The anaphase-promoting complex/cyclosome (APC/C) is a key target of the spindle checkpoint.

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Background: Proper regulation of the cohesion at the centromeres of human chromosomes is essential for accurate genome transmission. Exactly how cohesion is maintained and is then dissolved in anaphase is not understood.

Principal Findings: We have investigated the role of the cohesin complex at centromeres in human cells both by depleting cohesin subunits using RNA interference and also by expressing a non-cleavable version of the Rad21 cohesin protein.

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