14.3. Insect chitin synthase genes CHS-A and CHS-B are specialized for synthesis of epidermal cuticle and midgut peritrophic matrix

Muthukrishnan, Subbaratnam; Arakane, Yasuyuki; Hogenkamp, David G.; Specht, Charles A.; Beeman, Richard W.; Kanost, Michael R.; Kramer, Karl J.; Zimoch, Lars; Merzendorfer, Hans

doi:10.1016/j.cbpa.2007.06.144

Cited by 3 publications

(2 citation statements)

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“…1 A–C) and (2) there are two classes of chitin synthases, A and B, produced at the end of the pathway. In Tribolium castaneum, cuticular chitin synthesis is tied to chitin synthase A, while peritrophic membrane chitin synthesis is tied to chitin synthase B (Arakane et al 2005 ; Muthukrishnan et al 2007 ; Khajuria et al 2010 ). There are also several genes/proteins linked specifically to either cuticular structures or peritrophic membrane structures (Fig.…”

Section: Why Chitin? – the Physiological Basis Of Defensesmentioning

confidence: 99%

“…There are also several genes/proteins linked specifically to either cuticular structures or peritrophic membrane structures (Fig. 1 D; Muthukrishnan et al 2007 ; Chaudhari et al 2011 ). These links emerge largely in the context of understanding the diversity of arthropod life cycles and center around interactions between ecdysone and JH management of the two forms of Chitin Synthase and the Broad-Complex, Met, and Kruppel-Homolog (Zhou et al 1998 ; Zhou and Riddiford 2001 , 2002 ; Erezyilmaz et al 2005 , 2006 , 2009 ; Minakuchi et al 2008 ).…”

Section: Why Chitin? – the Physiological Basis Of Defensesmentioning

confidence: 99%

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A shared mechanism of defense against predators and parasites: chitin regulation and its implications for life‐history theory

Beckerman

Roij

Dennis

et al. 2013

Ecology and Evolution

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Defenses against predators and parasites offer excellent illustrations of adaptive phenotypic plasticity. Despite vast knowledge about such induced defenses, they have been studied largely in isolation, which is surprising, given that predation and parasitism are ubiquitous and act simultaneously in the wild. This raises the possibility that victims must trade-off responses to predation versus parasitism. Here, we propose that arthropod responses to predators and parasites will commonly be based on the endocrine regulation of chitin synthesis and degradation. The proposal is compelling because many inducible defenses are centered on temporal or spatial modifications of chitin-rich structures. Moreover, we show how the chitin synthesis pathway ends in a split to carapace or gut chitin, and how this form of molecular regulation can be incorporated into theory on life-history trade-offs, specifically the Y-model. Our hypothesis thus spans several biological scales to address advice from Stearns that “Endocrine mechanisms may prove to be only the tip of an iceberg of physiological mechanisms that modulate the expression of genetic covariance”.

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Section: Why Chitin? – the Physiological Basis Of Defensesmentioning

confidence: 99%