In vivo NMR as a tool for probing molecular structure and dynamics in intact Chlamydomonas reinhardtii cells

GO biological process enrichment for the 882 deletion strains below the threshold of detection by microarray in the BCprot relative to the gene universe of strains present in at least one deletion collectio

Mutations in <i>zfp-1</i> or <i>lin-35</i> enhance axon guidance defects in an <i>oxIs12</i>-dependent manner.

<p>A: The <i>zfp-1</i>(op481) point mutation, the <i>zfp-1</i>(ok554) deletion and <i>lin-35</i>(n745) lead to a very similar enhancement of defects when combined with <i>sdn-1</i>(zh20) or <i>hse-5</i>(tm472). However <i>zfp-1</i>(ok554) and <i>lin-35</i>(n745) are not enhancing each other. The defects of <i>zfp-1</i>(ok554)<i>; sdn-1</i>(zh20) and <i>lin-35</i>(n745)<i>; sdn-1</i>(zh20) disappear if <i>oxIs12</i> is replaced by either <i>oxIs268</i> or <i>juIs76</i>. B: Attempts to reconstitute the defects. (i) <i>pkIs296</i> enlarges the X-chromosome of <i>oxIs268; zfp-1</i>(ok554)<i>; sdn-1</i>(zh20) animals leading to a slight increase in defects, however not to the level of <i>zfp-1</i>(ok554)<i>; sdn-1</i>(zh20) <i>oxIs12</i> animals (ii). The <i>dpy-21</i>(e428) mutation behaves the same as <i>zfp-1</i> or <i>lin-35</i> mutations. The <i>dpy-21</i>(e428)<i>; sdn-1</i>(zh20) double mutant has severe D-type axon guidance defects if <i>oxIs12</i> is present but not if <i>oxIs268</i> is used to stain the D-type motor neurons. The phenotypes of <i>zfp-1</i>(ok554)<i>; sdn-1</i>(zh20) and <i>lin-35</i>(n745)<i>; sdn-1</i>(zh20) with either <i>oxIs12</i> or <i>juIs76</i> are shown as comparison. Grey bars represent the number of commissural axons growing away from the VNC; white bars indicate the number of commissural axons reaching the DNC. Dashed lines indicate limits according to Figure 1A. Numbers are from 50 L1 animals +/- SEM. Statistical test results are indicated as follows: ns = not significant, * = p<0.05, ** = p<0.005, *** = p<0.0005. Superscripts (also shown in the bars of the corresponding strains) indicate to which strain the comparison was made: 1: <i>hse-5</i>(tm472), 2: <i>sdn-1</i>(zh20), 3: <i>zfp-1</i>(ok554), 4: <i>zfp-1</i>(ok554)<i>; sdn-1</i>(zh20)<i>; oxIs268</i>, 5: <i>dpy-21</i>(e428)<i>; sdn-1</i>(zh20) <i>oxIs12</i>, 6: <i>zfp-1</i>(ok554)<i>; sdn-1</i>(zh20) <i>oxIs12</i>, 7: <i>lin-35</i>(n745)<i>; sdn-1</i>(zh20) <i>oxIs12</i>. The table summarizes the different transgenes used, indicates their composition and the chromosome in which they are integrated.</p

An HSPG network influences D-type motor axon guidance.

<p>A: Summary of relevant single and double mutants. All the single mutants have no or only minor defects, meaning that on average no more than one commissural axon fails to reach the dorsal nerve cord (DNC). The dashed line at 5 commissures per animal indicates the limit separating the single mutants from the weak enhancers. Weak enhancers (one to two commissural axons fail to reach the DNC, limit indicated by dashed line at 4 commissures per animal) are double mutants that are considered not to play an important role in D-type axon guidance. Strong enhancers have very clear D-type axon guidance defects (the dashed line at 2 commissures per animal is to allow for distant bars to be visually comparable). Statistical test results are indicated as follows: ns = not significant, * = p<0.05, ** = p<0.005, *** = p<0.0005. Superscripts (also shown in the bars of the corresponding strains) indicate to which strain the comparison was made: 1: <i>hse-5</i>(tm472), 2: <i>sdn-1</i>(zh20), 3: <i>cle-1</i>(cg120), 4: <i>hst-2</i>(ok595), 5: <i>lon-2</i>(e678) <i>sdn-1</i>(zh20). B-E: Representative pictures of wild type (B), <i>sdn-1</i>(zh20) (C) and <i>hse-5</i>(tm472) (D) single mutants and the strongest enhancer <i>hse-5</i>(tm472)<i>; sdn-1</i>(zh20) (E). The transgene <i>oxIs12</i> is present in all backgrounds. F: HSPG core proteins and HS modifying enzymes can be placed into two groups based on the strength of the D-type motor axon guidance defects observed in double mutants. Only the double mutants of the group of strong enhancers are considered for this network. For a complete set of strains see Figure S2. Grey bars in A represent the number of commissural axons growing away from the ventral nerve cord (VNC); white bars indicate the number of commissural axons reaching the DNC. Numbers are from 50 L1 animals +/- SEM.</p

Factors involved in dorsal axon guidance of D-type motor neurons.

<p>The two UNC-5 ligands UNC-6 (red) and UNC-129 (blue) form opposing gradients with high concentrations of UNC-6 ventrally and high UNC-129 concentrations on the dorsal side of the worm. The ventrally outgrowing growth cone (green) initially uses the UNC-5 receptor to respond to high UNC-6 concentrations. The more the growth cone approaches the dorsal side, the lower the UNC-6 concentration becomes while the concentration of UNC-129 increases, which is thought to induce a switch in UNC-6 signaling in the growth cone to UNC-5 + UNC-40 signaling. This enables the growth cone to maintain its response to the repulsive UNC-6 signal [24]. The HSPG SDN-1 is expressed in the neuron [5] and requires HST-6 function to modify its HS chains. SDN-1 could, through its HS chains, influence the interaction of UNC-6 and/or UNC-129 with UNC-5. Our genetic data suggest that PTP-3 is playing a role in this process too, but it remains an open question what its precise function is. Furthermore UNC-53 is involved in cytoskeletal remodeling [52] and MAX-1 [34] and ZAG-1 [57] are transcription factors with a possible function in the neuron. The HSPG LON-2 is expressed in the hypodermis [50]. Its function could be to establish and/or maintain the gradients of UNC-6 and/or UNC-129 to provide an ideal substrate for the growth cone on its way to the dorsal side. For this function LON-2 requires the enzymes HST-2, HSE-5 and HST-6 to modify its HS chains. Underlined protein names indicate that these genes are located on the X chromosome.</p

Oligonucleotide Array Comparative Genomic Hybridization (oaCGH) based characterization of genetic deficiencies as an aid to gene mapping in -3

<p><b>Copyright information:</b></p><p>Taken from "Oligonucleotide Array Comparative Genomic Hybridization (oaCGH) based characterization of genetic deficiencies as an aid to gene mapping in "</p><p>http://www.biomedcentral.com/1471-2164/8/402</p><p>BMC Genomics 2007;8():402-402.</p><p>Published online 7 Nov 2007</p><p>PMCID:PMC2220004.</p><p></p>) Predicted insertion of the duplicated region into the genome. (?) Unconfirmed deficiency structure

Oligonucleotide Array Comparative Genomic Hybridization (oaCGH) based characterization of genetic deficiencies as an aid to gene mapping in -1

<p><b>Copyright information:</b></p><p>Taken from "Oligonucleotide Array Comparative Genomic Hybridization (oaCGH) based characterization of genetic deficiencies as an aid to gene mapping in "</p><p>http://www.biomedcentral.com/1471-2164/8/402</p><p>BMC Genomics 2007;8():402-402.</p><p>Published online 7 Nov 2007</p><p>PMCID:PMC2220004.</p><p></p>us balancer. Colored bars beneath schematic indicate expected DNA ratios. (C-E) oaCGH data obtained in GFF file format for three balanced deficiency strains visualized using the SignalMap™ browser software [20]. (C) BC4697 (, (D) BC4638 (and (E) BC4690 (. Regions covered by are represented as blue lines above the data; deletions are represented by red lines below the data. (F) Expansion of oaCGH data across the left breakpoint region of . Region of deletion ambiguity is represented by broken lines. *Apparent internal duplications of

Fijnspar, Picea abies (L.) Karst. : morfologische kenmerken en selectie in Nederland

<p><b>Copyright information:</b></p><p>Taken from "Oligonucleotide Array Comparative Genomic Hybridization (oaCGH) based characterization of genetic deficiencies as an aid to gene mapping in "</p><p>http://www.biomedcentral.com/1471-2164/8/402</p><p>BMC Genomics 2007;8():402-402.</p><p>Published online 7 Nov 2007</p><p>PMCID:PMC2220004.</p><p></p>by RNAi phenotype are numbered. Identified mutation positions are shown in gene expansions

Oligonucleotide Array Comparative Genomic Hybridization (oaCGH) based characterization of genetic deficiencies as an aid to gene mapping in -4

<p><b>Copyright information:</b></p><p>Taken from "Oligonucleotide Array Comparative Genomic Hybridization (oaCGH) based characterization of genetic deficiencies as an aid to gene mapping in "</p><p>http://www.biomedcentral.com/1471-2164/8/402</p><p>BMC Genomics 2007;8():402-402.</p><p>Published online 7 Nov 2007</p><p>PMCID:PMC2220004.</p><p></p>by RNAi phenotype are numbered. Identified mutation positions are shown in gene expansions

Chromosome Movements Promoted by the Mitochondrial Protein SPD-3 Are Required for Homology Search during <i>Caenorhabditis elegans</i> Meiosis

<div><p>Pairing of homologous chromosomes during early meiosis is essential to prevent the formation of aneuploid gametes. Chromosome pairing includes a step of homology search followed by the stabilization of homolog interactions by the synaptonemal complex (SC). These events coincide with dramatic changes in nuclear organization and rapid chromosome movements that depend on cytoskeletal motors and are mediated by SUN-domain proteins on the nuclear envelope, but how chromosome mobility contributes to the pairing process remains poorly understood. We show that defects in the mitochondria-localizing protein SPD-3 cause a defect in homolog pairing without impairing nuclear reorganization or SC assembly, which results in promiscuous installation of the SC between non-homologous chromosomes. Preventing SC assembly in <i>spd-3</i> mutants does not improve homolog pairing, demonstrating that SPD-3 is required for homology search at the start of meiosis. Pairing center regions localize to SUN-1 aggregates at meiosis onset in <i>spd-3</i> mutants; and pairing-promoting proteins, including cytoskeletal motors and polo-like kinase 2, are normally recruited to the nuclear envelope. However, quantitative analysis of SUN-1 aggregate movement in <i>spd-3</i> mutants demonstrates a clear reduction in mobility, although this defect is not as severe as that seen in <i>sun-1(jf18)</i> mutants, which also show a stronger pairing defect, suggesting a correlation between chromosome-end mobility and the efficiency of pairing. SUN-1 aggregate movement is also impaired following inhibition of mitochondrial respiration or dynein knockdown, suggesting that mitochondrial function is required for motor-driven SUN-1 movement. The reduced chromosome-end mobility of <i>spd-3</i> mutants impairs coupling of SC assembly to homology recognition and causes a delay in meiotic progression mediated by HORMA-domain protein HTP-1. Our work reveals how chromosome mobility impacts the different early meiotic events that promote homolog pairing and suggests that efficient homology search at the onset of meiosis is largely dependent on motor-driven chromosome movement.</p></div

Additional file 11: Supplemental Data S3. of Rapid Increase in frequency of gene copy-number variants during experimental evolution in Caenorhabditis elegans

List of ORFs contained in eight overlapping duplications and deletions in experimental C. elegans lines following 180–212 generations of population expansion under competitive conditions. Duplication/deletion breakpoint coordinates and ORFs contained therein are based on Wormbase version WS243. (PDF 116 kb