12 research outputs found
The Secreted Immunoglobulin Domain Proteins ZIG-5 and ZIG-8 Cooperate with L1CAM/SAX-7 to Maintain Nervous System Integrity
During nervous system development, neuronal cell bodies and their axodendritic projections are precisely positioned through transiently expressed patterning cues. We show here that two neuronally expressed, secreted immunoglobulin (Ig) domain-containing proteins, ZIG-5 and ZIG-8, have no detectable role during embryonic nervous system development of the nematode Caenorhabditis elegans but are jointly required for neuronal soma and ventral cord axons to maintain their correct position throughout postembryonic life of the animal. The maintenance defects observed upon removal of zig-5 and zig-8 are similar to those observed upon complete loss of the SAX-7 protein, the C. elegans ortholog of the L1CAM family of adhesion proteins, which have been implicated in several neurological diseases. SAX-7 exists in two isoforms: a canonical, long isoform (SAX-7L) and a more adhesive shorter isoform lacking the first two Ig domains (SAX-7S). Unexpectedly, the normally essential function of ZIG-5 and ZIG-8 in maintaining neuronal soma and axon position is completely suppressed by genetic removal of the long SAX-7L isoform. Overexpression of the short isoform SAX-7S also abrogates the need for ZIG-5 and ZIG-8. Conversely, overexpression of the long isoform disrupts adhesion, irrespective of the presence of the ZIG proteins. These findings suggest an unexpected interdependency of distinct Ig domain proteins, with one isoform of SAX-7, SAX-7L, inhibiting the function of the most adhesive isoform, SAX-7S, and this inhibition being relieved by ZIG-5 and ZIG-8. Apart from extending our understanding of dedicated neuronal maintenance mechanisms, these findings provide novel insights into adhesive and anti-adhesive functions of IgCAM proteins
The Small, Secreted Immunoglobulin Protein ZIG-3 Maintains Axon Position in Caenorhabditis elegans
Vertebrate and invertebrate genomes contain scores of small secreted or transmembrane proteins with two immunoglobulin (Ig) domains. Many of them are expressed in the nervous system, yet their function is not well understood. We analyze here knockout alleles of all eight members of a family of small secreted or transmembrane Ig domain proteins, encoded by the Caenorhabditis elegans zig (âzwei Ig DomĂ€nenâ) genes. Most of these family members display the unusual feature of being coexpressed in a single neuron, PVT, whose axon is located along the ventral midline of C. elegans. One of these genes, zig-4, has previously been found to be required for maintaining axon position postembryonically in the ventral nerve cord of C. elegans. We show here that loss of zig-3 function results in similar postdevelopmental axon maintenance defects. The maintenance function of both zig-3 and zig-4 serves to counteract mechanical forces that push axons around, as well as various intrinsic attractive forces between axons that cause axon displacement if zig genes like zig-3 or zig-4 are deleted. Even though zig-3 is expressed only in a limited number of neurons, including PVT, transgenic rescue experiments show that zig-3 can function irrespective of which cell or tissue type it is expressed in. Double mutant analysis shows that zig-3 and zig-4 act together to affect axon maintenance, yet they are not functionally interchangeable. Both genes also act together with other, previously described axon maintenance factors, such as the Ig domain proteins DIG-1 and SAX-7, the C. elegans ortholog of the human L1 protein. Our studies shed further light on the use of dedicated factors to maintain nervous system architecture and corroborate the complexity of the mechanisms involved
<i>zig-5</i> and <i>zig-8</i> affect axon positioning in the ventral nerve cord.
<p>(A) PVQ axon flip-over (red arrowhead) in <i>zig-5 zig-8</i> double mutants, observed first in later larval stages, but not earlier. Ventral view, anterior is to the left. Grey arrows indicate the location of axon flip-over. Scale bar is 5 ”m. (B) Quantification of axon flip-over defects in <i>zig-5 zig-8</i> double mutants, using transgenes <i>oyIs14, hdIs29, bwIs2, oxIs12</i> and <i>zdIs13</i>, respectively. Single mutants <i>zig-5</i> and <i>zig-8</i> are wild type <a href="http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.1002819#pgen.1002819-Benard3" target="_blank">[11]</a>. Animals were paralyzed with <i>unc</i> mutants or levamisole (Lev). Proportions of different animal populations were compared using the z-test. â*â indicates p<0.01.</p
Rescue of <i>zig-5 zig-8</i> mutant phenotypes.
1<p>On top of or anterior to nerve ring. Scored with <i>oyIs14 (sra-6::gfp)</i>.</p>2<p>Repeated from <a href="http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.1002819#pgen-1002819-g001" target="_blank">Figure 1</a> for comparison.</p>3<p>Compared to non-transgenic control (74% defective). Injection of <i>zig-5</i> and <i>zig-8</i> expressed under the control of a number of neuronal or pharyngeal promoters, at a range of concentrations, did not produce better rescue of the mutant phenotypes than that obtained with the fosmid and YAC.</p
The <i>zig-5</i> and <i>zig-8</i> soma positioning defects are maintenance defects.
<p>(A) Soma displacement defects in <i>zig-5 zig-8</i> animals are only apparent at late larval and adult stages. See legend to <a href="http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.1002819#pgen-1002819-g001" target="_blank">Figure 1C</a> for explanation of symbols. <i>Scale</i> bar is 5 ”m. (B) Quantification of ASI and ASH neuronal displacement in <i>zig-5 zig-8</i> double mutants at different developmental stages and when paralyzed in <i>unc</i> mutant backgrounds or on the drug levamisole (Lev). Proportions of different animal populations were compared using the z-test. â*â indicates p<0.001.</p
Neuronal maintenance factors and the defects caused by their removal.
<p>(A) Schematic protein structures and alleles used in this study. (B) Summary of previous <i>in vitro</i> and <i>in vivo</i> adhesion studies <a href="http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.1002819#pgen.1002819-Sasakura1" target="_blank">[6]</a>, <a href="http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.1002819#pgen.1002819-Pocock1" target="_blank">[7]</a>. Star indicates a shortened hinge region which prevents formation of the horseshoe configuration <a href="http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.1002819#pgen.1002819-Pocock1" target="_blank">[7]</a>. (C) ASI and ASH neuronal displacements observed in <i>zig-5(ok1065)</i> and <i>zig-8(ok561)</i> single and double mutant adult animals with the <i>oyIs14</i> reporter transgene. Blue arrowheads indicate position of the nerve ring and red arrowheads position of neuronal soma, which is scored relative to position of the nerve ring (wild type: behind nerve ring; mutant: on top of to nerve ring). Anterior to left, dorsal on top. Scale bar is 5 ”m. (D) Quantification of ASI and ASH neuronal displacement in single and double mutants of the <i>zig</i> gene family. Alleles are described in <a href="http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.1002819#pgen.1002819-Benard3" target="_blank">[11]</a>. Error bars indicate s.e.p.. Proportions of different animal populations were compared using the z-test. â*â indicates p<0.001.</p
Genetic interactions between <i>zig-5, zig-8</i> and <i>sax-7</i>.
<p>(A) ASI and ASH neuronal displacements in mutant adult animals scored with the <i>oyIs14</i> reporter transgene. Wild-type and <i>zig-5 zig-8</i> double mutant pictures are the same as shown in <a href="http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.1002819#pgen-1002819-g001" target="_blank">Figure 1C</a> and shown for comparison only. See legend to <a href="http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.1002819#pgen-1002819-g001" target="_blank">Figure <i>1C</i></a> for explanation of symbols. <i>Scale</i> bar is 5 ”m. (B) Quantification of ASI and ASH neuronal position in genetic different backgrounds. âpunc-14â is a panneuronal driver. <i>Punc-14::sax-7L</i>: DNA was injected at 75 ng/uL (line 1) or 50 ng/uL (lines 2 and 3). <i>Punc-14::sax-7S and Punc-14::sax7Î11</i>: DNA was injected at 50 ng/uL. Proportions of different animal populations were compared using the z-test. â*â indicates p<0.001. (C) Genetic interactions of <i>zig-5, zig-8</i> and <i>sax-7</i> in controlling axon positioning in the ventral nerve cord. Quantification of PVQ axon flip-overs with transgene <i>oyIs14</i>. Error bars indicate s.e.p. Proportions of different animal populations were compared using the z-test. â*â indicates p<0.01. (D) Effect of ectopic expression of various forms of <i>sax-7</i> in a wild-type background. ASI and ASH neuronal position are quantified. Proportions of different animal populations were compared using the z-test. â*â indicates p<0.001. (E) Quantification of ASI and ASH neuronal position in <i>dig-1(ky188)</i> mutant animals. â<i>Punc-14</i>â is a panneuronal driver for expression of SAX-7S. There are no statistically significant differences between <i>dig-1</i> animals and any of the transgenic <i>dig-1</i> animals expressing <i>sax-7S.</i></p
Genetic interactions of <i>zig-5, zig-8</i> and <i>sax-7</i>.
<p>This figure summarizes the genetic interaction data described in this paper.</p
The Secreted Immunoglobulin Domain Proteins ZIG-5 and ZIG-8 Cooperate with L1CAM/SAX-7 to Maintain Nervous System Integrity
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Global dataset of soil organic carbon in tidal marshes.
Funder: The Nature Conservancy through the Bezos Earth Fund and other donor supportFunder: Nelson Mandela UniversityFunder: State Research Agency of Spain (AEI; CGL2007-64915), the Mancomunidad de los Canales del Taibilla (MCT), and the Science and Technology Agency of the Murcia Region (Seneca Foundation; 00593/PI/04 & 08739/PI/08).Funder: Scottish Government and UK Natural Environment Research Council C-SIDE project (grant NE/R010846/1)Funder: COOLSTYLE/CARBOSTORE projectFunder: New Zealand Ministry for Business, Innovation and Employment Contract #C01X2109Funder: Portuguese national funds from FCT - Foundation for Science and Technology through projects UIDB/04326/2020, UIDP/04326/2020, LA/P/0101/2020, and 2020.03825.CEECINDFunder: German Research Foundation (DFG project number: GI 171/25-1)Funder: State Research Agency of Spain (AEI; CGL2007-64915), the Mancomunidad de los Canales del Taibilla (MCT), the Science and Technology Agency of the Murcia Region (Seneca Foundation; 00593/PI/04 & 08739/PI/08), and a RamĂłn y Cajal contract from the Spanish Ministry of Science and Innovation (RYC2020-029322-I)Funder: Velux foundation (#28421, BlĂ„ Skove â Havets Skove som kulstofdrĂŠn)Funder: LIFE ADAPTA BLUES project Ref. LIFE18 CCA/ES/001160Funder: LIFE ADAPTA BLUES project Ref. LIFE18 CCA/ES/001160, support of national funds through Fundação para a CiĂȘncia e Tecnologia, I.P. (FCT), under the projects UIDB/04292/2020, UIDP/04292/2020, granted to MARE, and LA/P/0069/2020, granted to the Associate Laboratory ARNETFunder: Financial support provided by the Welsh Government and Higher Education Funding Council for Wales through the SĂȘr Cymru National Research Network for Low Carbon, Energy and Environment; as well as the Spanish Ministry of Science and Innovation (project PID2020-113745RB-I00) and FEDERFunder: South African Department of Science and Innovation (DSI)âNational Research Foundation (NRF) Research Chair in Shallow Water Ecosystems (UID: 84375), and the Nelson Mandela UniversityFunder: I+D+i projects RYC2019-027073-I and PIE HOLOCENO 20213AT014 funded by MCIN/AEI/10.13039/501100011033 and FEDERFunder: Funding support from the Scottish Government and UK Natural Environment Research Council C-SIDE project (grant NE/R010846/1)Funder: Xunta de Galicia (GRC project IN607A 2021-06)Funder: U.S. Army Engineering, Research and Development Center (ACTIONS project, W912HZ2020070)Tidal marshes store large amounts of organic carbon in their soils. Field data quantifying soil organic carbon (SOC) stocks provide an important resource for researchers, natural resource managers, and policy-makers working towards the protection, restoration, and valuation of these ecosystems. We collated a global dataset of tidal marsh soil organic carbon (MarSOC) from 99 studies that includes location, soil depth, site name, dry bulk density, SOC, and/or soil organic matter (SOM). The MarSOC dataset includes 17,454 data points from 2,329 unique locations, and 29 countries. We generated a general transfer function for the conversion of SOM to SOC. Using this data we estimated a median (± median absolute deviation) value of 79.2â±â38.1 Mg SOC ha-1 in the top 30âcm and 231â±â134 Mg SOC ha-1 in the top 1âm of tidal marsh soils globally. This data can serve as a basis for future work, and may contribute to incorporation of tidal marsh ecosystems into climate change mitigation and adaptation strategies and policies