50 Years of Women in Cell Biology: Where have we been? Where are we going?

It's been 50 years since Women in Cell Biology (WICB) was founded by junior women cell biologists who found themselves neither represented at the American Society for Cell Biology (ASCB) presentations nor receiving the information, mentoring, and sponsorship they needed to advance their careers. Since then, gender parity at ASCB has made significant strides: WICB has become a standing ASCB committee, women are regularly elected president of the ASCB, and half the symposia speakers are women. Many of WICB's pioneering initiatives for professional development, including career panels, workshops, awards for accomplishments in science and mentoring, and career mentoring roundtables, have been incorporated and adapted into broader "professional development" that benefits all members of ASCB.

The Science and Value of Diversity: Closing the Gaps in Our Understanding of Inclusion and Diversity.

Diversity drives excellence. Diversity enhances innovation in biomedical sciences and, as it relates to novel findings and treatment of diverse populations, in the field of infectious diseases. There are many obstacles to achieving diversity in the biomedical workforce, which create challenges at the levels of recruitment, retention, education, and promotion of individuals.

Invisible woman?

The number of invited women speakers at scientific meetings is much less than their proportion in a field. This means that women have fewer venues to present their research, less opportunity to increase their professional network, and smaller chances of promotion and financial support. The paucity of women speakers also sends a message to aspiring young female researchers that there is no room for them at the top.

Mutations in PDGFRB cause autosomal-dominant infantile myofibromatosis.

Infantile myofibromatosis (IM) is a disorder of mesenchymal proliferation characterized by the development of nonmetastasizing tumors in the skin, muscle, bone, and viscera. Occurrence within families across multiple generations is suggestive of an autosomal-dominant (AD) inheritance pattern, but autosomal-recessive (AR) modes of inheritance have also been proposed. We performed whole-exome sequencing (WES) in members of nine unrelated families clinically diagnosed with AD IM to identify the genetic origin of the disorder.

Women in cell biology: a seat at the table and a place at the podium.

The Women in Cell Biology (WICB) committee of the American Society for Cell Biology (ASCB) was started in the 1970s in response to the documented underrepresentation of women in academia in general and cell biology in particular. By coincidence or causal relationship, I am happy to say that since WICB became a standing ASCB committee, women have been well represented in ASCB's leadership and as symposium speakers at the annual meeting. However, the need to provide opportunities and information useful to women in developing their careers in cell biology is still vital, given the continuing bias women face in the larger scientific arena.

TGF-β-stimulated CTGF production enhanced by collagen and associated with biogenesis of a novel 31-kDa CTGF form in human corneal fibroblasts.

Purpose: Connective tissue growth factor (CTGF) is induced by transforming growth factor-beta (TGF-β) after corneal wounding. This study addressed the role of the extracellular matrix in the induction of CTGF by TGF-β.

Methods: Human corneal fibroblasts (HCFs) were grown on fibronectin (FN), vitronectin (VN), or collagen (CL) in supplemented serum-free media alone or with TGF-β1 or fibroblast growth factor plus heparin.

Urokinase receptor cleavage: a crucial step in fibroblast-to-myofibroblast differentiation.

Fibroblasts migrate into and repopulate connective tissue wounds. At the wound edge, fibroblasts differentiate into myofibroblasts, and they promote wound closure. Regulated fibroblast-to-myofibroblast differentiation is critical for regenerative healing.

Localization of ZO-1 in the nucleolus of corneal fibroblasts.

Purpose: Within the multidomain structure of ZO-1 are motifs responsible for ZO-1's localization to intercellular junctions and its newly demonstrated localization to the leading edge of lamellipodia in corneal fibroblasts. Since ZO-1 also has two nuclear localization signals, this study was undertaken to determine whether stimuli associated with wounding would induce nuclear translocation of ZO-1

Methods: Immunocytochemistry and immunoblot analysis were used to localize endogenous and exogenous ZO-1 in nuclear and cytoplasmic sites in corneal fibroblasts and 293T fibroblasts, with and without myc-ZO-1 transfection. Cells were serum starved by growth for 48 hours in DMEM/F12 with 0.

FAK-dependent regulation of myofibroblast differentiation.

Fibroblasts and myofibroblasts both participate in wound healing. Transforming growth factor beta (TGFbeta) induces fibroblasts to differentiate into myofibroblasts, whereas fibroblast growth factor and heparin (FGF/h) induce myofibroblasts to "de-differentiate" into fibroblasts. TGFbeta induces expression of smooth muscle alpha actin (SMalphaA) and incorporation into in stress fibers, a phenotype of differentiated myofibroblasts.

ZO-1: lamellipodial localization in a corneal fibroblast wound model.

Purpose: To explore the roles of ZO-1 in corneal fibroblasts and myofibroblasts in a model of wounding.

Methods: Antibodies were used to identify ZO-1 in cultured rabbit corneal fibroblasts by immunocytochemistry, Western blot analysis, and immunoprecipitation. For colocalization studies, antibodies to beta-catenin, cadherins, connexins, integrins, alpha-actinin, and cortactin were used.

Urokinase anchors uPAR to the actin cytoskeleton.

Purpose: To investigate the expression and localization of urokinase plasminogen activator (uPA) and its receptor (uPAR) and their interaction with the actin cytoskeleton in human corneal fibroblasts.

Methods: Primary cultured human corneal fibroblasts were exposed to exogenous uPA to investigate its effect on the distribution of uPAR under resting conditions and in a scrape-wound model. Fluorescence microscopy, immunolocalization, immunoprecipitation, and the actin depolymerizing drug cytochalasin D were used to evaluate uPAR's interaction with the actin cytoskeleton.

Involvement of S100A4 in stromal fibroblasts of the regenerating cornea.

Purpose: S100A4 is a member of the S100 family of calcium-binding proteins. Members of the S100 family have been implicated in a variety of cellular events, including growth, signaling, differentiation, and motility. It has been suggested that S100A4 modulates cell shape and motility by interacting with components of the cytoskeleton.