The use of personal response systems, or clickers, is increasingly common in college classrooms. Although clickers can increase student engagement and discussion, their benefits also can be overstated. A common practice is to ask the class a question, display the responses, allow the students to discuss the question, and then collect the responses a second time. In an introductory biology course, we asked whether showing students the class responses to a question biased their second response. Some sections of the course displayed a bar graph of the student responses and others served as a control group in which discussion occurred without seeing the most common answer chosen by the class. If students saw the bar graph, they were 30% more likely to switch from a less common to the most common response. This trend was more pronounced in true/false questions (38%) than multiple-choice questions (28%). These results suggest that observing the most common response can bias a student's second vote on a question and may be misinterpreted as an increase in performance due to student discussion alone.
Double strand breaks (DSBs) have been found at several meiotic recombination hot spots in Saccharomyces cerevisiae; more global studies have found that they occur at many places along several yeast chromosomes during meiosis. Indeed, the number of breaks found is consistent with the number of recombination events predicted from the genetic map. We have previously demonstrated that the HIS2 gene is a recombination hot spot, exhibiting a high frequency of gene conversion and associated crossing over. This paper shows that DSBs occur in meiosis at a site in the coding region and at a site downstream of the HIS2 gene and that the DSBs are dependent upon genes required for recombination. The frequency of DSBs at HIS2 increases when the gene conversion frequency is increased by alterations in the DNA around HIS2, and vice versa. A deletion that increases both DSBs and conversion can stimulate both when heterozygous; that is, it is semidominant and acts to stimulate DSBs in trans. These data are consistent with the view that homologous chromosomes associate with each other before the formation of the DSBs.The mechanism whereby homologous chromosomes find each other during meiosis and initiate recombination has been the source of considerable speculation and experimentation. Several models have been proposed to account for the genetic and, more recently, molecular data that have been obtained about meiotic recombination. The classical Holliday model (1) suggested that nicks are made in strands of the same polarity in two homologs, after which the broken strands are exchanged from one duplex to the other. The Meselson-Radding model (2) begins recombination with a single strand nick on one homolog, after which one end of the broken strand invades the homologous duplex. More recently, the double strand break (DSB) model for recombination was proposed by Szostak et al. (3); in this scheme, both ends of the broken duplex invade the homolog to initiate recombination. In the latter two models, one can imagine that the mechanism whereby homologs find each other involves recA-like (4) synaptase-assisted searching by the single strands created at the initiating breaks or nicks.Since the publication of the DSB model, experiments have been done that demonstrate that DSBs occur during meiosis in yeast and that they are associated with recombination. These experiments may be sorted into two groups: (i) experiments that examine recombination hot spots both for recombination and DSBs, and (ii) experiments that look at the more global distribution of DSBs along entire chromosomes. Within the first class of experiments, Sun et al. (5) first demonstrated that a meiotic DSB occurs at the ARG4 locus. The location of the DSB was in the DNA sequences that had been shown to be necessary (6) for conversion at ARG4. Furthermore, the time at which the breaks appeared was consistent with the time at which commitment to recombination occurred. In these early experiments, the DSBs were difficult to detect, in part because they were transien...
In the yeast, Saccharomyces cerevisiae, several genes appear to act early in meiotic recombination. HOPl and REDl have been classified as such early genes. The data in this paper demonstrate that neither a redl nor a hopl mutation can rescue the inviable spores produced by a rad52 spol3 strain; this phenotype helps to distinguish these two genes from other early meiotic recombination genes such as SPOll, REC104, or A4EI4. In contrast, either a redl or a hopl mutation can rescue a rad50S spol3 strain; this phenotype is similar to that conferred by mutations in the other early recombination genes (e.g., REC104). These two different results can be explained because the data presented here indicate that a rad50S mutation does not diminish meiotic intrachromosomal recombination, similar to the mutant phenotypes conferred by redl or hopl. Of course, REDl and HOPl do act in the normal meiotic interchromosomal recombination pathway; they reduce interchromosomal recombination to ~10% of normal levels. We demonstrate that a mutation in a gene (REC104) required for initiation of exchange is completely epistatic to a mutation in REDl. Finally, mutations in either HOPl or RED1 reduce the number of doublestrand breaks observed at the HIS2 meiotic recombination hotspot.
Using a selection based upon the ability of early Rec- mutations (e.g., rad50) to rescue the meiotic lethality of a rad52 spo13 strain, we have isolated 177 mutants. Analysis of 56 of these has generated alleles of the known Rec genes SPO11, ME14 and MER1, as well as defining five new genes: REC102, REC104, REC107, REC113 and REC114. Mutations in all of the new genes appear to specifically affect meiosis; they do not have any detectable mitotic phenotype. Mutations in REC102, REC104 and REC107 reduce meiotic recombination several hundred fold. No alleles of RED1 or HOP1 were isolated, consistent with the proposal that these genes may be primarily involved with chromosome pairing and not exchange.
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