Sea urchin membrane transport mechanisms for calcificationand pH homeostasis
Larval sea urchins serve as a model organism for calcification and adult individuals are a keystone species in marine shelf ecosystems. Both life stages will presumably be affected by alterations of seawater pCO2 and the accompanying change in pH, [HCO3-] and [CO32-]. This change in seawater carbona...
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| Other Authors: | , |
| Format: | Doctoral or Postdoctoral Thesis |
| Language: | English |
| Published: |
2013
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| Online Access: | https://nbn-resolving.org/urn:nbn:de:gbv:8-diss-124088 https://macau.uni-kiel.de/receive/diss_mods_00012408 https://macau.uni-kiel.de/servlets/MCRFileNodeServlet/dissertation_derivate_00004903/Dissertation%20Holtmann%202013_druckreif.pdf |
| Summary: | Larval sea urchins serve as a model organism for calcification and adult individuals are a keystone species in marine shelf ecosystems. Both life stages will presumably be affected by alterations of seawater pCO2 and the accompanying change in pH, [HCO3-] and [CO32-]. This change in seawater carbonate chemistry is known as ocean acidification and is based on anthropogenically caused increase in pCO2 by burning fossil fuels and deforestation. Ocean acidification is thought to affect marine organisms in terms of acid-base regulation but also in terms of calcification, somatic growth and reproductivity. To understand the impact of ocean acidification on calcification processes a profound knowledge of the underlying cellular mechanisms is needed. This thesis is split into two main topics: cellular mechanisms involved in sea urchin larval calcification, and ocean acidification related effects on skeletal elements and mechanisms for acid-base regulation of the perivisceral coelomic fluid (PCF) in adult sea urchins. To understand more about the cellular mechanisms involved in sea urchin calcification, larvae of Strongylocentrotus droebachiensis were raised in the presence of different ion transport protein inhibitors and the primary body rod length of pluteus larvae was taken as a measure for calcification. This investigation challenged the current cell model of sea urchin ion transport. The model had been developed on the basis of high drug concentrations which partially resulted in toxic side effects on larval development. The inhibitors used in this study targeted the Na+K+2Cl- cotransporter (NKCC), L-type Ca2+ channel, Ca2+ ATPase, anion exchangers (SLC4-family), H+K+ ATPase and V-ATPase. I could show that loop diuretics inhibited calcification selectively and could prove that NKCC is expressed in sea urchin larvae. In addition, the function of the cotransporter in the primary mesenchyme cells (PMCs) was addressed and it could be shown that this transporter is needed for maintaining the cytoplasmic cord, i.e. the ... |
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