High impact information on HOXA13

• To elucidate the function of Hoxa-13 that is expressed in the autopod during normal limb development, Hoxa-13 was misexpressed in the entire limb bud with a replication-competent retroviral system [1].
• Misexpression of Hoxa-13 resulted in a remarkable size reduction of the zeugopodal cartilages as a result of the arrest of cartilage cell growth and differentiation restricted in the zeugopod [1].
• These results indicate that Hoxa-13 is responsible for switching the genetic code from long bone formation to short bone formation during normal development [1].
• Administration of BMP-2 at the anterior margin of the limb bud induced ectopic HOXA-13 expression in the anterior region of the muscle masses followed by ectopic muscle formation close to the source of exogenous BMP-2 [2].
• We found that HOXA-13 expression in the autopodal mesenchyme was dependent on the AER but not on the polarizing region, whereas expression of HOXA-13 in the posterior muscle masses was dependent on the polarizing region but not on the AER [2].

Biological context of HOXA13

• We dissected the regulatory mechanisms directing the unique expression patterns of Hoxa-11 and Hoxa-13 during limb muscle development [2].

Anatomical context of HOXA13

• Under the influence of the limb mesenchyme, Hoxa-11 is expressed in migrating and proliferating premyoblasts in the limb field and Hoxa-13 is induced in subdomains of congregated limb muscle masses [3].
• Forced expression of Hoxa-13 resulted in more pronounced repression of MyoD in both limb and C2C12 myoblasts [3].
• Misexpression of Hoxa-13 induces cartilage homeotic transformation and changes cell adhesiveness in chick limb buds [1].

Associations of HOXA13 with chemical compounds

• In contrast, targeted disruption of Hoxa-13 gave rise to enhanced expression of MyoD in the flexor carpi radialis muscle, a forearm muscle that normally expressed Hoxa-13 [3].

Regulatory relationships of HOXA13

• These results suggested that HOXA-13 expression in the posterior muscle masses is activated by the posteriorizing signal from the posterior mesenchyme via BMP-2 [2].

Other interactions of HOXA13

• Thus, mesenchymal HOXA-13 expression was independent of BMP-2 from polarizing region, but was under the control of as yet unidentified signals from the AER [2].
• The expression of Hoxd-12, Hoxd-13 and Hoxa-13 genes was maintained in the recombinants, indicating that these cells carry information about their autopodial origin, and this correlates well with their distal restricted morphogenetic potential [4].
• Contrary to the model, addition of FGF4 to early limb buds does not activate Hoxa13 prematurely nor extend the Hoxa13 expression domain proximally [5].

References