YARSI UNIVERSITY PROGRAM TO MEET THE DEMAND OF STUDENT’S ENGLISH FLUENCY WITH TOEIC AS THE ASSESSMENT TOOL

Abstract: A test is only a measurement tool of a learning process. The important part is the learning process itself; how the process can help learners acquire English as a foreign language that enables them to compete in the working environment. To measure the process, TOEIC with all its parts was meant to measure learners’ ability to communicate in English. Teachers should not be focusing on the test but more on the approaches that allow the students to have adequate and sophisticated listening, reading, and writing skills to exchange information and to negotiate meaning in real life. Many university level English teachers are trapped within the rules that students should achieve a 550 or 605 TOEIC score to graduate. Instead of helping the students to acquire the language as a communication tool, they tend to focus more on getting the students to master the test. This is what teachers should deal with, not only facilitate students to learn the language but at the same time help them to do the test well. Despite the challenge of facing students who lack motivation and have very basic English skills, Yarsi University Language Lab is setting up several programs and approaches that allow students to acquire the language and enable them to communicate in the target language which is eventually measured by an instrument called TOEIC. Keywords: Language Acquisition, direct and indirect test, discrete and intregativ

cis-reQTL mapping and <i>SLC45A2</i> reQTL.

<p>(A) Outline of the approach for mapping cis-reQTLs (B) QQ plot of the cis-reQTL p-value for all genes tested. Red indicates the top 3 genes discussed in the text and used in subsequent analyses. (C) Normalized fold change of <i>SLC45A2</i> expression separated by genotype at the cis-reQTL (rs12653176). p-value calculated from the Spearman correlation. (D) Normalized <i>SLC45A2</i> expression of the NSE and SE samples separated by genotype at the same locus. p-values calculated from the Spearman correlation. (E) Manhattan plot of the fold change (FC), NSE sample expression, and SE sample expression associations with all SNPs one megabase surrounding <i>SLC45A2</i>. p-values calculated from the Spearman correlation.</p

Sun-exposed and non-sun-exposed skin samples.

<p>(A) First and second principal components of all GTEx samples with selected tissue-types highlighted by color. (B) First and second principal components using all genes in only the skin samples. (C) Fold enrichment of 2-fold differentially expressed genes from Choi <i>et al</i>. [<a href="http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.1006382#pgen.1006382.ref043" target="_blank">43</a>] as a function of the stringency in calling differentially expressed genes from the GTEx samples.</p

Differential cis-eQTL mapping and validation with ASE.

<p>(A) Outline of our approach to mapping differential cis-regulation. (B) The expression of <i>SIM2</i> for each exposure-type after segregation by genotype at the eQTL (rs2248813). P-values are from the asymptotic approximation of the Spearman correlation (rho). (C) ASE validation of the <i>SIM2</i> result for individuals heterozygous at the eQTL. The allele on the y-axis indicates the allele at the eQTL (see x-axis of panel B), and the ASE directionalities were phased based on these alleles. * indicates p-value < 0.05 by t-test. (D) QQ plot of each tested gene after combining the effect size test and the differential ASE test. Red indicates the gene had a significant GxE expression interaction with a SNP (FDR < 0.05, Benjamini-Hochberg).</p

Testing se-eQTLs for signs of local adaptation.

<p>Environmental correlations with allele frequency in (A) HGDP populations and (B) Lazaridis et al [<a href="http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.1006382#pgen.1006382.ref062" target="_blank">62</a>] populations. Left panels: Heatmap of the environmental variables used in the study. Units are Watts per meter squared. Populations are marked with blue circles. Note that three of the American populations from Lazaridis <i>et al</i>. (Mixe, Mixtec, and Zapotec) [<a href="http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.1006382#pgen.1006382.ref062" target="_blank">62</a>] are marked in the same geographic location. Right panels: Radiation level vs allele frequency of the population for the <i>RASSF9</i> se-eQTL (rs11117173) with the color indicating the regional subgroup. For each regional subgroup, the Spearman correlation (Rho), the number of individuals (Ind), and the number of populations (Pop) are provided in the table.</p

A polygenic gene expression adaptation in the ergosterol biosynthesis (ERG) pathway.

<p>(<b>A</b>) The final steps of the ERG pathway. Eight genes whose down-regulation contributes to a polygenic gene expression adaptation are colored red; the six previously implicated genes <a href="http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.1003813#pgen.1003813-Fraser4" target="_blank">[8]</a> are underlined. Erg28 is shown next to its strongest interaction partner, Erg27. (<b>B</b>) Allelic bias of ERG genes, as measured by pyrosequencing in the RM/BY hybrid. The allelic bias indicates the magnitude of <i>cis-</i>regulatory divergence between RM and BY for each gene. Red color indicates genes that are part of the polygenic adaptation. Asterisks indicate those that interact strongly with Erg28 <a href="http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.1003813#pgen.1003813-Mo1" target="_blank">[24]</a>, all of which have stronger allelic bias than those that do not.</p

Determining the molecular mechanism of the causal mutation.

<p>(<b>A</b>) Two predicted transcription factor (TF) binding sites flanking the deletion. (<b>B</b>) The expected fold-change in <i>ERG28</i> expression level when deleting TFs under different scenarios. Left: if a TF does not regulate <i>ERG28</i>, its deletion should have no effect on <i>ERG28</i> levels. Center: If a TF regulates <i>ERG28</i> and acts independently of the two-base deletion, then deleting the TF should result in some fold-change X, which will be observed in both the wildtype RM and RM AA112Δ backgrounds. Right: If a TF regulates the wildtype <i>ERG28</i> promoter, but the deletion abolishes this regulation, then the TF deletion may only affect <i>ERG28</i> mRNA levels in the wildtype background (A fourth possible scenario, not shown, is where the TF only regulates <i>ERG28</i> in RM AA112Δ). (<b>C</b>) qPCR data showing changes in <i>ERG28</i> mRNA levels upon deleting either <i>SOK2</i> or <i>MOT3</i>. In both cases, a difference is observed in the wildtype background (<i>p</i> = 7.5×10⁻⁵ for <i>SOK2</i> and 5.0×10⁻³ for <i>MOT3</i>), but not the RM AA112Δ background (<i>p</i> = 0.28 for <i>SOK2</i> and 0.67 for <i>MOT3</i>), consistent with the TF regulation being entirely abolished by the deletion. (<b>D</b>) Chromatin immunoprecipitation data showing the difference in binding for Sok2 and Mot3 to the <i>ERG28</i> promoter in wildtype RM/RM AA112Δ. In both cases a significant decrease in binding is observed in RM AA112Δ.</p

Pinpointing the causal mutation affecting <i>ERG28 cis</i>-regulation.

<p>(<b>A</b>) Sequence divergence between RM and BY in the <i>ERG28</i> promoter region. No other differences exist for 590 bp upstream of the gene, or in the 5′ UTR. (<b>B</b>) Genotypes at the two variable positions for RM, BY, and the two engineered strains. (<b>C</b>) The mRNA levels of <i>ERG28</i> in each of the two engineered strains compared to wildtype RM, assayed by qPCR. The causal mutation is expected to result in a ∼1.30-fold difference, matching the allelic bias observed in the RM/BY hybrid (<a href="http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.1003813#pgen-1003813-g001" target="_blank">Figure 1B</a>), whereas any non-causal mutation will not alter the RM expression level (∼1-fold change). (<b>D</b>) Allelic expression bias in hybrids between each engineered strain and BY, assayed by pyrosequencing. Any non-causal mutation will not alter the 1.30-fold RM/BY allelic bias, whereas the causal mutation is expected to be expressed at the same level as the BY allele (∼1-fold allelic bias).</p