Pharyngeal pumping rate does not reflect lifespan extension in transgenerational longevity mutants.

Epigenetic modifications must be reprogrammed with each new generation. In , defects in histone methylation reprogramming allow for the transgenerational acquisition of longevity. For example, mutations in the putative H3K9 demethylase JHDM-1 extend lifespan after six to ten generations.

C. elegans Gonad Dissection and Freeze Crack for Immunofluorescence and DAPI Staining.

The C. elegans germline makes an excellent model for studying meiosis, in part due to the ease of conducting cytological analyses on dissected animals. Whole mount preparations preserve the structure of meiotic nuclei, and importantly, each gonad arm contains all stages of meiosis, organized in a temporal-spatial progression that makes it easy to identify nuclei at different stages.

establishes germline versus soma by balancing inherited histone methylation.

Formation of a zygote is coupled with extensive epigenetic reprogramming to enable appropriate inheritance of histone methylation and prevent developmental delays. In , this reprogramming is mediated by the H3K4me2 demethylase SPR-5 and the H3K9 methyltransferase, MET-2. In contrast, the H3K36 methyltransferase MES-4 maintains H3K36me2/3 at germline genes between generations to facilitate re-establishment of the germline.

Hansel, Gretel, and the Consequences of Failing to Remove Histone Methylation Breadcrumbs.

Like breadcrumbs in the forest, cotranscriptionally acquired histone methylation acts as a memory of prior transcription. Because it can be retained through cell divisions, transcriptional memory allows cells to coordinate complex transcriptional programs during development. However, if not reprogrammed properly during cell fate transitions, it can also disrupt cellular identity.

Repressive H3K9me2 protects lifespan against the transgenerational burden of COMPASS activity in .

In , mutations in WDR-5 and other components of the COMPASS H3K4 methyltransferase complex extend lifespan and enable its inheritance. Here, we show that mutant longevity is itself a transgenerational trait that corresponds with a global enrichment of the heterochromatin factor H3K9me2 over twenty generations. In addition, we find that the transgenerational aspects of mutant longevity require the H3K9me2 methyltransferase MET-2, and can be recapitulated by removal of the putative H3K9me2 demethylase JHDM-1.

The Pipeline CURE: An Iterative Approach to Introduce All Students to Research Throughout a Biology Curriculum.

Participation in research provides personal and professional benefits for undergraduates. However, some students face institutional barriers that prevent their entry into research, particularly those from underrepresented groups who may stand to gain the most from research experiences. Course-based undergraduate research experiences (CUREs) effectively scale research availability, but many only last for a single semester, which is rarely enough time for a novice to develop proficiency.

A Model for Epigenetic Inhibition via Transvection in the Mouse.

Transvection is broadly defined as the ability of one locus to affect its homologous locus Although it was first discovered in the 1950s, there are only two known cases in mammals. Here, we report another instance of mammalian transvection induced by the / system, which is widely used for conditional gene targeting in the mouse. We attempted to use the germline-expressed transgene to engineer a mouse mutation, but observe a dramatic reduction of recombination in mice that inherit an already deleted allele A similar phenomenon has previously been observed with another that is expressed during meiosis: This second example of inhibition reinforces the conclusion that certain meiotically expressed alleles can initiate transvection in mammals.

Making evolution stick: using sticky notes to teach the mechanisms of evolutionary change.

Evolution and its mechanisms of action are concepts that unite all aspects of biology, but remain some of the most difficult for students to understand. To address this challenge, we designed a hands-on activity that introduces fundamental mechanisms of evolutionary change: natural selection, genetic drift, and gene flow. In small groups, students use a population of sticky notes to reveal the consequences of each mechanism on phenotype frequency.

End joining at Caenorhabditis elegans telomeres.

Critically shortened telomeres can be subjected to DNA repair events that generate end-to-end chromosome fusions. The resulting dicentric chromosomes can enter breakage-fusion-bridge cycles, thereby impeding elucidation of the structures of the initial fusion events and a mechanistic understanding of their genesis. Current models for the molecular basis of fusion of critically shortened, uncapped telomeres rely on PCR assays that typically capture fusion breakpoints created by direct ligation of chromosome ends.