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pxn-1 and pxn-2 May Interact Negatively during Neuronal Development and Aging in C. elegans.

Cho I, Hwang GJ, Cho JH - Mol. Cells (2015)

Bottom Line: In addition, pxn-2 overexpressing animals retained an intact neuronal morphology when compared with age-matched controls.Consistent with these results, overexpression of both pxn-1 and pxn-2 restored the severe neuronal defects present with pxn-1 overexpression.These results implied that there is a negative relationship between pxn-1 and pxn-2 via pxn-1 regulating pxn-2.

View Article: PubMed Central - PubMed

Affiliation: Department of Biology Education, College of Education, Chosun University, Gwangju 501-759, Korea.

ABSTRACT
C. elegans has two functional peroxidasins (PXN), PXN-1 and PXN-2. PXN-2 is essential to consolidate the extracellular matrix during development and is suggested to interact with PXN-1 antagonistically. pxn-1 is involved in neuronal development and possibly maintenance; therefore, we investigated the relationship between pxn-1 and pxn-2 in neuronal development and in aging. During neuronal development, defects caused by pxn-1 overexpression were suppressed by overexpression of both pxn-1 and pxn-2. In neuronal aging process, pxn-1 mutants showed less age-related neuronal defects, such as neuronal outgrowth, neuronal wavy processes, and enhanced short-term memory performance. In addition, pxn-2 overexpressing animals retained an intact neuronal morphology when compared with age-matched controls. Consistent with these results, overexpression of both pxn-1 and pxn-2 restored the severe neuronal defects present with pxn-1 overexpression. These results implied that there is a negative relationship between pxn-1 and pxn-2 via pxn-1 regulating pxn-2. Therefore, pxn-1 may function in neuronal development and age-related neuronal maintenance through pxn-2.

No MeSH data available.


Related in: MedlinePlus

pxn-1 and pxn-2 double overexpression suppresses the effect of pxn-1 overexpression in developing neurons. (A) Neuronal defects during development are presented as the percentage of the total number of neurons counted in overexpressing animals: control (juIs76 [Punc-25::gfp]), pxn-1 overexpression (Ppxn-1::pxn-1), pxn-2 overexpression (Ppxn-2::pxn-2), and pxn-1 and pxn-2 overexpression (Ppxn-1::pxn-1+Ppxn-2::pxn-2). (B) Neuronal defects during development are presented as a percentage in various ectopic overexpressing worms: Phs::gfp, pxn-1 overexpression (Phs::pxn-1), pxn-2 overexpression (Phs::pxn-2), and pxn-1 and pxn-2 over-expression (Phs::pxn-1+Phs::pxn-2). All experiments were performed in juIs76 background. n > 300 worms per line. Error bar = STD. *p < 0.01; Student’s t-test.
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f1-molce-38-8-729: pxn-1 and pxn-2 double overexpression suppresses the effect of pxn-1 overexpression in developing neurons. (A) Neuronal defects during development are presented as the percentage of the total number of neurons counted in overexpressing animals: control (juIs76 [Punc-25::gfp]), pxn-1 overexpression (Ppxn-1::pxn-1), pxn-2 overexpression (Ppxn-2::pxn-2), and pxn-1 and pxn-2 overexpression (Ppxn-1::pxn-1+Ppxn-2::pxn-2). (B) Neuronal defects during development are presented as a percentage in various ectopic overexpressing worms: Phs::gfp, pxn-1 overexpression (Phs::pxn-1), pxn-2 overexpression (Phs::pxn-2), and pxn-1 and pxn-2 over-expression (Phs::pxn-1+Phs::pxn-2). All experiments were performed in juIs76 background. n > 300 worms per line. Error bar = STD. *p < 0.01; Student’s t-test.

Mentions: Overexpression of pxn-1 in worms results in more prominent neuronal defects during development than in pxn-1 mutants (Lee et al., 2015); therefore, we used pxn-1 overexpressing worms with either its own promoter or a heat shock promoter to assess neuronal defects (Figs.1A and 1B). Consistent with our previous study, pxn-1 overexpression (Ppxn-1::pxn-1) resulted in increased axonal defects when compared with control worms (74 and 36%, respectively; Fig. 1A). pxn-2 overexpressing worms (Ppxn-2::pxn-2) showed slightly increased defects (44%; Fig. 1A). The overexpression of both pxn-1 and pxn-2 (Ppxn-1::pxn-1+Ppxn-2::pxn-2) attenuated the neuronal defects when compared with pxn-1 overexpression alone (47%; Fig. 1A). There was a 45% recovery of neuronal defects in pxn-1;pxn-2 double overexpressing worms when compared with pxn-1 overexpressing worms. These results were replicated using the ectopic overexpressing animals, Phs::pxn-1, Phs:: pxn-2, and Phs::pxn-1 + Phs::pxn-2 (Fig. 1B). The recovery pattern of double overexpressing animals was similar between ectopic and cis-overexpression, although the rate differed (45% and 21% in cis- and ectopic overexpression, respectively). These results suggested that pxn-1 has an antagonistic relationship with pxn-2 in neuronal development, which is consistent with the results of Gotenstein et al. (2010).


pxn-1 and pxn-2 May Interact Negatively during Neuronal Development and Aging in C. elegans.

Cho I, Hwang GJ, Cho JH - Mol. Cells (2015)

pxn-1 and pxn-2 double overexpression suppresses the effect of pxn-1 overexpression in developing neurons. (A) Neuronal defects during development are presented as the percentage of the total number of neurons counted in overexpressing animals: control (juIs76 [Punc-25::gfp]), pxn-1 overexpression (Ppxn-1::pxn-1), pxn-2 overexpression (Ppxn-2::pxn-2), and pxn-1 and pxn-2 overexpression (Ppxn-1::pxn-1+Ppxn-2::pxn-2). (B) Neuronal defects during development are presented as a percentage in various ectopic overexpressing worms: Phs::gfp, pxn-1 overexpression (Phs::pxn-1), pxn-2 overexpression (Phs::pxn-2), and pxn-1 and pxn-2 over-expression (Phs::pxn-1+Phs::pxn-2). All experiments were performed in juIs76 background. n > 300 worms per line. Error bar = STD. *p < 0.01; Student’s t-test.
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f1-molce-38-8-729: pxn-1 and pxn-2 double overexpression suppresses the effect of pxn-1 overexpression in developing neurons. (A) Neuronal defects during development are presented as the percentage of the total number of neurons counted in overexpressing animals: control (juIs76 [Punc-25::gfp]), pxn-1 overexpression (Ppxn-1::pxn-1), pxn-2 overexpression (Ppxn-2::pxn-2), and pxn-1 and pxn-2 overexpression (Ppxn-1::pxn-1+Ppxn-2::pxn-2). (B) Neuronal defects during development are presented as a percentage in various ectopic overexpressing worms: Phs::gfp, pxn-1 overexpression (Phs::pxn-1), pxn-2 overexpression (Phs::pxn-2), and pxn-1 and pxn-2 over-expression (Phs::pxn-1+Phs::pxn-2). All experiments were performed in juIs76 background. n > 300 worms per line. Error bar = STD. *p < 0.01; Student’s t-test.
Mentions: Overexpression of pxn-1 in worms results in more prominent neuronal defects during development than in pxn-1 mutants (Lee et al., 2015); therefore, we used pxn-1 overexpressing worms with either its own promoter or a heat shock promoter to assess neuronal defects (Figs.1A and 1B). Consistent with our previous study, pxn-1 overexpression (Ppxn-1::pxn-1) resulted in increased axonal defects when compared with control worms (74 and 36%, respectively; Fig. 1A). pxn-2 overexpressing worms (Ppxn-2::pxn-2) showed slightly increased defects (44%; Fig. 1A). The overexpression of both pxn-1 and pxn-2 (Ppxn-1::pxn-1+Ppxn-2::pxn-2) attenuated the neuronal defects when compared with pxn-1 overexpression alone (47%; Fig. 1A). There was a 45% recovery of neuronal defects in pxn-1;pxn-2 double overexpressing worms when compared with pxn-1 overexpressing worms. These results were replicated using the ectopic overexpressing animals, Phs::pxn-1, Phs:: pxn-2, and Phs::pxn-1 + Phs::pxn-2 (Fig. 1B). The recovery pattern of double overexpressing animals was similar between ectopic and cis-overexpression, although the rate differed (45% and 21% in cis- and ectopic overexpression, respectively). These results suggested that pxn-1 has an antagonistic relationship with pxn-2 in neuronal development, which is consistent with the results of Gotenstein et al. (2010).

Bottom Line: In addition, pxn-2 overexpressing animals retained an intact neuronal morphology when compared with age-matched controls.Consistent with these results, overexpression of both pxn-1 and pxn-2 restored the severe neuronal defects present with pxn-1 overexpression.These results implied that there is a negative relationship between pxn-1 and pxn-2 via pxn-1 regulating pxn-2.

View Article: PubMed Central - PubMed

Affiliation: Department of Biology Education, College of Education, Chosun University, Gwangju 501-759, Korea.

ABSTRACT
C. elegans has two functional peroxidasins (PXN), PXN-1 and PXN-2. PXN-2 is essential to consolidate the extracellular matrix during development and is suggested to interact with PXN-1 antagonistically. pxn-1 is involved in neuronal development and possibly maintenance; therefore, we investigated the relationship between pxn-1 and pxn-2 in neuronal development and in aging. During neuronal development, defects caused by pxn-1 overexpression were suppressed by overexpression of both pxn-1 and pxn-2. In neuronal aging process, pxn-1 mutants showed less age-related neuronal defects, such as neuronal outgrowth, neuronal wavy processes, and enhanced short-term memory performance. In addition, pxn-2 overexpressing animals retained an intact neuronal morphology when compared with age-matched controls. Consistent with these results, overexpression of both pxn-1 and pxn-2 restored the severe neuronal defects present with pxn-1 overexpression. These results implied that there is a negative relationship between pxn-1 and pxn-2 via pxn-1 regulating pxn-2. Therefore, pxn-1 may function in neuronal development and age-related neuronal maintenance through pxn-2.

No MeSH data available.


Related in: MedlinePlus